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| Journal of the New Zealand Medical Association,
23-January-2009, Vol 122 No 1288
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Prevalence of undiagnosed diabetes, impaired glucose
tolerance, and impaired fasting glucose among Māori in Te Wai o Rona:
Diabetes Prevention Strategy
David Simmons, Elaine Rush, Nic Crook
The management of known Type 2 diabetes and its
complications accounts for a significant proportion of health expenditure in New
Zealand.1 However, much of diabetes remains
undiagnosed2 and levels of hyperglycaemia below
the diagnostic threshold for diabetes (impaired glucose tolerance [IGT] and
impaired fasting glucose [IFG]) are also associated with an excess risk of
cardiovascular disease.3 Such levels of
hyperglycaemia are also at high risk of progressing to Type 2 diabetes,
progression now known to be preventable by intensive lifestyle change and some
medications.4–6
The potential benefits of detecting any abnormal glucose
tolerance vary between populations depending on risk of developing diabetes and
risk of complications once diabetes has been diagnosed. Calculating the costs
and benefits of intervening at an early stage require detailed information
including the proportion with undiagnosed diabetes, IGT and IFG.
Māori have higher rates of diabetes than European New
Zealanders and disproportionately higher rates of many of the complications
caused by diabetes.2 As such, a successful
diabetes prevention strategy among Māori is crucial for New Zealand and
Māori alike.
Te Wai o Rona: Diabetes Prevention Strategy was a 4-year
randomised controlled trial among Māori communities in the Waikato and
Lakes District Health Board areas,7 registered
with the Australasian Controlled Trials Registry (ACTRN012605000622606). The
trial did not proceed after the first 3 years for funding reasons. However, the
baseline data, being population based may be able to be used to provide the
needed detailed information regarding the proportion with undiagnosed diabetes,
IGT, and IFG and we now present these data and discuss the caveats behind the
data.
MethodsParticipants—All Māori
resident within the boundaries of the Waikato DHB, and the tribal area of Ngati
TuWharetoa in the neighbouring Lakes DHB were invited to participate with their
families. The age cutoff for entry was taken as ≥28 years on 30 September
2005. Recruitment was by personal invitation from local general practitioners in
association with media releases (television, radio, posters, newspapers)
announcing times/venues of screening, workplace screening, and personal contact.
Personal
contact through different health organisations and their staff, and
announcements at a number of Māori community activities became increasingly
important through the recruitment phase. Those who attended were asked to inform
other family members and friends.
Participants were asked to attend after a 10-hour
overnight fast and were advised that breakfast would be provided. Advice was
also given that attending non-fasting was also acceptable although full testing
(including OGTT) would not then be performed. Those unfit to sign a consent
form, with terminal disease, or not permanently residing in the study area at
the time of the baseline data collection were excluded.
Ethical approval was provided by both the Waikato and
Bay of Plenty Ethics Committees. All participants gave signed informed
consent.
Screening sessions were held 0700–1400 hours in a
variety of community venues across the study area. Where possible, transport was
provided for participants. After registration/consent and ascertainment of
fasting status, fasting participants had a finger-prick glucose (venous plasma
equivalent) using a glucose meter (Advantage, Roche, Switzerland) and
venesection. Those who were non-fasting had a single venesection for glucose and
HbA1c (Bio-rad Diamat Variant, [upper limit of reference range 6.4%], Bio-Rad
Laboratories, USA).
Samples for HbA1c were sent to the same laboratory for
analysis. Glucose samples were centrifuged, separated, and refrigerated within
30 minutes on site in a mobile laboratory and subsequently measured using the
Hitachi 911 (Hitachi Limited, Tokyo, Japan). All assays were within target
limits specified by the RCPA Quality Assurance Program. These assays were
carried out by the Waikato District Health Board Laboratory which has IANZ
ISO9002 Accreditation.
Fasting participants with a fingerprick glucose
≥4.4 mmol/L were advised to undertake a 75g 2 hour oral glucose tolerance
test (OGTT), although those with values below this were also invited to have an
OGTT.
Trained staff facilitated standard questionnaire and
measurement completion. Questionnaires including demographic data were
completed. Ethnicity was determined by self identity. During the OGTT, other
measurements included height±0.5 cm (portable height scale PE087; Mentone
Education Centre, Victoria, Australia) and weight±0.1 kg (Wedderburn
TI-TH316 Personal scales or Wedderburn TI-BWB800 Personal scales [up to 200kg]
for oversize participants).
Based upon previous research including
Māori,8 if no OGTT had been completed and
the fasting glucose was ≥5.3 mmol/L, or a random glucose ≥5.3 mmol/L
or the HbA1c ≥ 5.3%, participants were asked to subsequently attend the
local community laboratory for an OGTT (screen positive subjects).
Screen-negative subjects were defined as those with
HbA1c, fasting, and random glucose results below these criteria. Diabetes, IFG,
and IGT were diagnosed using 1998 World Health Organization
criteria.9 If no OGTT was undertaken and the
fasting glucose was ≥7.0 mmol/L and/or the random glucose was ≥11.1
mmol/L, diabetes was considered to be present.
Statistics—The overall
prevalence of diabetes (among those aged ≥30 years) was calculated by
direct age standardization to the 2006
Census.10 Comparisons are made by either
Chi-squared test or by comparing 95% confidence intervals. Tests are 2-tailed
with p<0.05 taken as significant. Mantell Haenszel test was used to
compare the prevalence of dysglycaemia by community services card use, after
adjustment for age and gender.
ResultsOf the 5059 non-pregnant adults screened for diabetes, 4269
were Māori aged ≥28 years (approximately 13% of the comparably aged
Māori population in the recruitment
area).10
Figure 1 shows the attendance at OGTT (n=3784) including
among those with a negative screen. Among screened Māori, 2726 (63.9%) were
women, the mean age was 48±12 years, 67.4% were rural residents, and 65.9%
were known to have a family member with diabetes. Very few (3.7%) of those with
a negative screen had IGT and none had diabetes or IFG.
Figure 1. Response to screening and crude
proportions with diabetes, impaired glucose tolerance (IGT), and impaired
fasting glucose (IFG)
 Among men, 86.7% and 79.2% of those above and below the
criteria for OGTT respectively had an OGTT, the proportions being 85.2% and
89.9% respectively among women. Among those not attending OGTT and
screen-positive (above the threshold for OGTT), 15 were considered to have
diabetes on the basis of their screening test.
Among the screen-positive participants, the fasting blood
glucose (n=109), random blood glucose (n=338), and HbA1c were similar between
those attending and not attending OGTT (5.3±0.9 vs 5.5±2.1 mmol/L;
5.5±1.0 vs 5.6±1.8 mmol/L; 6.0±0.6 vs 6.0±1.0%
respectively). As the proportion with a “negative screen” was small
(4.5%), and most of these had an OGTT (among whom few had IGT and none with
diabetes or IFG), analyses assume that the negative screen group were all normal
and that those not having an OGTT were comparable to the overall cohort.
Age-specific prevalence is therefore calculated from those who had an OGTT or
who were screen negative without an OGTT (n=33).
Table 1 shows that the prevalence of diabetes increased with
age, although no Māori aged over 80 years was found to have undiagnosed
diabetes. The age standardised prevalence of undiagnosed diabetes was higher
among men than women (6.5[5.8–7.4]% vs 4.2[3.6–4.8]%), as was that
for IFG (5.4[4.7–6.1]% vs 3.0[2.3–3.5]%), but not IGT
(8.5[7.6–9.4]% vs 9.7[8.7–10.6]%).
Table 1. Response to screening and estimated
prevalence of undiagnosed diabetes, IGT, and IFG among Māori
Those who were screen negative were <15.0% in all
age-sex groups.
There was no significant difference in prevalence of
diabetes, IGT, or IFG between those living in rural and urban areas, nor between
those living in different rural tribal areas. Among those classified as having
diabetes, 12.8% had a fasting glucose <6.1 mmol/L and 8.2% had a fasting
glucose <5.6 mmol/L. Among those with IGT, 76.2% had a fasting glucose
<6.1 mmol/L and 46.7% had a fasting glucose <5.6 mmol/L.
Mean BMI
among women was 32.9±7.8 kg/m2 and among
men was 33.1±6.7 kg/m2. The prevalence of
diabetes, IGT, and IFG are shown by body mass index (BMI) group in Figure 2
(women) and Figure 3 (men). The BMI groups were defined by 1
kg/m2 across the overweight and obese ranges
(25–36 kg/m2).
There was no significant age difference between the BMI
groups. Prevalence of dysglycaemia increased with increasing BMI with no clear
inflection point. Among the 29.4% of women and 28.4% of men with a BMI ≥36
kg/m2, over one-third had some degree of
dysglycaemia, particularly IGT.
Figure 2. Prevalence of diabetes, IGT, and IFG
by body mass index (women)
 Figure 3. Prevalence of diabetes, IGT, and IFG
by body mass index (men)
 Note: The 1 subject with a BMI <19
kg/m2 had IGT.
The prevalence of dysglycaemia was 1.38(1.16–1.65)
fold greater among those with a community services card after age and gender and
1.33(1.11–1.60) fold greater after additionally adjusting for BMI.
Undiagnosed diabetes alone was 1.24(0.91–1.69) fold higher among those
with a community services card (i.e. non significant).
DiscussionThis is one of several studies reporting the prevalence of
undiagnosed diabetes, IGT, and IFG among Māori in different parts of New
Zealand.2 The prevalence of undiagnosed
diabetes was higher than in the Diabetes Heart and Health
Study11 and comparable to that in the Ngati and
Healthy Project.12
Abnormal glucose tolerance, particularly undiagnosed
diabetes, was particularly high among Māori men and the very obese. As
diabetes, IGT, and IFG remain harbingers of significant cardiovascular
disease,3 and lifestyle and pharmacological
intervention can significantly reduce the risk of future morbidity and
mortality, we need to find ways to identify such dysglycaemia as early as
possible.
Those identified as having diabetes in this study were
followed up for microvascular disease (retinopathy and nephropathy) and while
retinopathy was prevalent in very few, microalbuminuria and albuminuria were
present in 29.6% and 7.7% respectively.7
We have previously shown that microalbuminuria is often
present before diagnosis of diabetes in Māori and that it is more related
to the familial risk of renal disease than
diabetes.13 The low prevalence of retinopathy
was heartening and is a measure of the duration that individuals remained
undiagnosed.14
The prevalence of known diabetes in the area is unknown, and
the low rate of retinopathy at diagnosis might suggest a greater uptake of
screening in this district. A combined diabetes specialist clinic and retinal
screening register has estimated the prevalence of known diabetes among Waikato
Māori to be 1.4% (30–39 years), 4.0% (40–49 years), 10.9%
(50–59 years), and 17–20% (60+
years).15
These data exclude some important patients (e.g. those
attending eye clinic but not the diabetes specialist clinic) and are not
gender-specific, but suggest that (perhaps) over 50% of diabetes is undiagnosed
in those 30–49 years, but that 25–40% are undiagnosed over this age.
In view of the risk from undiagnosed Type 2 diabetes in
pregnancy among Māori women,16 and the
risk of renal disease and other long-term complications from uncontrolled
diabetes among Māori,2 diabetes screening
and diagnostic strategies among Māori under 50 years warrants greater
attention.
With such a high prevalence of undiagnosed diabetes shown in
these analyses, and the excess risk of cardiovascular disease associated with
dysglycaemia, there is clearly scope to increase identification of Māori
with any form of dysglycaemia, who would benefit from intervention.
Whether this would help address the higher mortality rates
among Māori, particularly Māori
men17, is yet to be seen. This difference is
known to be associated with greater deprivation, and in our study, use of a
community services card, accessible only to those on reduced incomes, was
associated with a greater prevalence of dysglycaemia. The lack of a significant
association with new diabetes was possibly due to insufficient statistical
power.
Of interest was the lack of difference in prevalence between
rural and urban Māori (as well as between tribal areas), suggesting a
balance between access to diabetes screening between rural and urban Māori
and actual diabetes/dysglycaemia risk.
We have carefully looked at the prevalence of IGT, IFG, and
undiagnosed diabetes in relation to obesity as measured by BMI. Naturally,
prevalence increased with increasing BMI, but there was no natural inflection
point to assist with defining obesity within Māori.
A range of studies have recommended that Māori have
different criteria for obesity using BMI in view of their lower fat content at a
given BMI.18 Clearly what is of importance in
defining a cut off for risk is relating the cutoff to a hard end point such as
diabetes or CVD. While such analyses should preferably be prospective using a
baseline BMI, in reality, BMI changes over time and a greater weight gain is
associated with greater diabetes risk.19
In our study, using cross-sectional data, there is no BMI
between 25 and 36 which would help define overweight or obesity. These data do
need to consider penetration of screening, which may have been greater among
more obese Māori.
There are a range of caveats to interpreting these data.
These are recruits into a trial of lifestyle change to prevent diabetes. We are
aware that some participants attended to be screened for diabetes (i.e. the
trial may have attracted those who were symptomatic). Conversely, those
attending for a lifestyle trial are possibly more likely to lead a healthier
life and to have started making healthier food and physical activity choices,
which would impact on risk of dysglycaemia.
Notwithstanding this self selection, the vast majority were
obese and hence this is unlikely to have had a major impact on the nature of the
cohort. The cohort represents approximately 25% of Māori women and <15%
of Māori men in the area, again suggesting that caution should be used in
extrapolating these findings to the wider local or national Māori
population.
One of the major strengths of the cohort is the high
proportion who underwent OGTT without reliance on a fasting test alone. The
criteria used to avoid OGTT were largely ignored by participants, resulting in a
high proportion of screen negative individuals having an OGTT. This was
important, with the high proportion of Māori with diabetes and IGT with a
lower fasting glucose. These data are important to inform future screening
campaigns and emphasising the importance of the OGTT in identifying those with
undiagnosed dysglycaemia who could benefit from intervention.
In conclusion, we have shown that undiagnosed diabetes, IGT,
and IFG remain common in this Māori cohort (particularly in men and the
very obese) and that there remains significant opportunity to reduce Māori
morbidity and premature mortality through case-finding and intervention.
Competing interests: None known.
Author information: David Simmons, Lead
Community Diabetologist, Institute of Metabolic Science, Cambridge University
Hospitals NHS Foundation Trust, Cambridge, England; Elaine Rush, Professor of
Nutrition, Centre for Physical Activity and Nutrition Research, AUT University,
Auckland, New Zealand; Nic Crook, Diabetes Consultant, Lakes District Health
Board, Rotorua, New Zealand
Funding and acknowledgements: Funding was
provided by Health Research Council, Waikato District Health Board, Lakes
District Health Board, Ministry of Health, Sport and Recreation New Zealand,
Southern Trust, Waikato Local Diabetes Team, and Merck Sharp and Dohme. Support
in kind was provided by Roche Diagnostics, Pathlab, Medlab, University of
Auckland, Auckland University of Technology, Wintec, Te Hotu Manawa Māori,
Eggs Inc, Vodafone, Rivermill Bakers, and Sun Fruit. We thank the investigator
group, Kaitiaki, Māori Community Health Workers, Te Wai o Rona: Diabetes
Prevention Strategy Project team, and local health service staff for their
varied contributions to the study. DS also thanks NIHR Cambridge Biomedical
Research Centre for its support.
Correspondence: Professor David Simmons,
Institute of Metabolic Science, Cambridge University Hospitals NHS Foundation
Trust, Cambridge, UK CB2 2QQ. Fax: +44 (0)1223 217080; Email: dsworkster@gmail.com
References:
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