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Epidemiology of diabetes in New Zealand: revisit to a
changing landscape
Grace Joshy, David Simmons
Almost a decade has passed since
Simmons1,2 painted the
portrait of diabetes epidemiology in New Zealand and warned about the increasing
risk of diabetes and its complications, especially for Māori and Pacific
peoples. When Moore and Lunt 3 re-examined the situation in 2000, they
found the burden of diabetes and its complications escalating, especially
end-stage renal failure (ESRF). They also noted the ageing population structure,
increasing Pacific population (mostly of Samoan, Tongan, Niuean, and Cook
Islands origin), and the obesity epidemic. Since this time, New Zealand’s
population has continued to age (median age has increased 2.5 years over 10
years). Furthermore, it has grown by 6%, with a 40% increase in the Asian
population (2001–2005).4 These figures point to an increasing Type 2
diabetes burden for New Zealand.
The New Zealand Ministry of Health has responded to the
growing diabetes epidemic with a diabetes strategic plan5 in 1997, a Diabetes
Implementation Plan6 in 2000, and a “Diabetes Toolkit”7 for district
health boards (DHBs) in 2001. The latter included the establishment of Local
Diabetes Teams at DHB level and the free
annual Get Checked programme for
diabetes patients. A set of guidelines for the management of Type 2 diabetes
were released in 2003.8 A Ministry of Health/ Health Research Council grant was
put out to tender in 2001 and again in 2003, which was subsequently awarded to
the Te Wai o Rona: Diabetes Prevention Strategy team in the Waikato/Lakes
districts.9
Results from a large number of important studies have been
published since the last review, which have confirmed the picture of a disease
increasing in numbers, especially at a younger age and consistent with a
lowering of the age at onset of Type 2 diabetes.
The aim of this review is to describe the current burden of
diabetes and the current district-based strategies underway to tackle a
condition likely to impact on the ability of New Zealand to afford other health
services.
MethodsA comprehensive review was undertaken using MEDLINE
database, reviewing diabetes prevalence or complications studies/surveys
reporting New Zealand-specific figures. Experimental intervention trials have
been excluded. The Australia and New Zealand Dialysis and Transplant Registry
(ANZDATA) Reports from 1990–2004, the MoH publications / reports, and New
Zealand Society for Study of Diabetes conference abstract books from 2000 have
been reviewed.
The latest unpublished results from the
Get Checked programme, being the only
national diabetes surveillance tool, were obtained from the MoH. The diabetes
teams in all DHBs were consulted via email regarding current (unpublished)
initiatives on diabetes control and prevention (10/21, 48% response). While a
comprehensive attempt has been made to include current unpublished diabetes
initiatives, there could be a limitation on the number of such initiatives
included in this article due to the limited
response.
Prevalence of diabetesAs with many other countries,25 currently there are no
up-to-date national diabetes prevalence data for New Zealand. The only area with
comprehensive epidemiological data is South Auckland, where between 1991 and
1995 a household survey of 100,000 residents was undertaken26 with a nested
study of those with undiagnosed diabetes undertaken thereafter.23
Table 1 shows the prevalence of diagnosed and undiagnosed
diabetes in different population-based surveys by ethnic group. As no
significant and consistent gender differences in prevalence have been found,27
prevalence data have been integrated.
Table 1. Prevalence (%) of known diabetes, undiagnosed
diabetes, and IGT/IFG in New Zealand by ethnicity
* Age standardised;
†
Crude prevalence, Europeans include Asians, Māori include Polynesians;
‡ Asians include others; §
Europeans include others; SADP=South Auckland Diabetes Project.
The SADP survey11 found a high prevalence of diabetes in the
non-European populations of New Zealand (except in Chinese and Cambodians); the
highest prevalence was found in South Asians—e.g. Asian Indians. (Figure
1). The prevalence of diabetes among Chinese was also low on the Middlemore
Hospital surgical wards19 at this time and has been shown in other Chinese
populations.28
The NZHS 2002/03 results showed an increased diabetes
prevalence of 8.4% among Asians living in New Zealand when compared with 1996/7,
although South Asians were also included in the Asian category.
Figure 1. Prevalence (%) of known (Type 1 and Type 2)
diabetes among 40–49 year olds in South Auckland (by ethnic
group)
![]() Source: South
Auckland Diabetes Project (SADP) survey, 1992–95.11 Middle East=e.g.
Iranians, Iraqis, Egyptians; South Asians=e.g. Indians, Sri Lankans,
Bangladeshi.
Compared with Europeans aged ≥40 years, the prevalence
of undiagnosed diabetes is more than three-fold among
Māori and more
than four-fold among Pacific
peoples.27
HbA1c screening of 50,819 subjects aged 20+ years found that Māori, Pacific
people, and Indians had particularly high rates of elevated HbA1c.
The age-standardised proportion of individuals with HbA1c
>6% in these ethnic groups were increased six-fold. Preliminary results from
Te Wai o Rona Diabetes Prevention Strategy24 in the Waikato are consistent with
the South Auckland data, but the age-specific prevalence of undiagnosed diabetes
was greater than predicted in the younger age groups.
Risk factor screening is still recommended in New Zealand,29
although many of those with undiagnosed
diabetes
(25.0%) and dysglycaemia (31.4%) have no
diabetes
risk factors.30
Past studies have indicated the earlier
onset of Type 2
diabetes in Māori (8–10 years earlier) and Pacific people (5–9
years earlier) than Europeans.31,32
The NZHS 1996/97 figures are in agreement with the results
from the SADP survey regarding age at diabetes diagnosis among Europeans
(50–55.5 years),
Māori (41–43 years), and Pacific (45–47 years)—but the
NZHS 2002/03 results for Māori and Pacific are contradictory (50 and 51
years respectively).
About 10–15% of diagnosed diabetes is Type 1 diabetes
among European New Zealanders; it is approximately 5% among other ethnic groups.
Of concern, the incidence of Type1 diabetes diagnosed before 20 years of age in
Canterbury, New Zealand has increased 3.4-fold in 30 years—from 6.79 to
22.79 patients/100,000 per year starting from 1970.33 This increase is
considered consistent with a worldwide increase in Type 1 diabetes.
In the most recent national study, Campbell-Stokes et al34
estimated the average annual incidence in 1999/2000 to be 17.9 per 100,000 (95%
CI: 15.9–20.0) among children under 15 years. Unlike earlier studies, this
study found that Māori, Pacific people, and Asians all had significantly
lower incidence rates (both absolute and relative to their respective population
proportions) than Europeans, although the basis of the ethnicity definition is
not stated.
Although the prevalence of Type 1 diabetes was found to be
lower in non-Europeans in a recent Christchurch study, they also noted the
increasing number of Māori, Pacific, and Asian people with
diabetes.20
Figure 2
shows the projected numbers with known diabetes by ethnic group across all
surveys to date, although the cross comparisons are limited by the changing
definitions of ethnicity and diabetes. Figure 2 also shows the different MOH
diabetes forecasts for New Zealand (based upon the NZHS 96–97 and South
Auckland Household Survey 91), which may be underestimates (e.g. the 2003
predictions were already less than the prevalence of diabetes among
Europeans, Pacific
peoples, and Māori males in the NZHS 2002/03 survey).
The age at onset of Type 2 diabetes has also been dropping,
with increasing numbers of children and adolescents with Type 2 diabetes and
women with Type 2 diabetes in pregnancy. The Auckland Diabetes Centre has
reported increasing prevalence of Type 2 diabetes in adolescents.36 The
prevalence of Type 2 diabetes among the adolescent clinic attendees was 1.8% in
1996, and 11.0% in 2002.
Northland
Diabetes Service has reported that Type 2 diabetes presents before the age of 30
years in 2.66% of Māori diagnosed with diabetes.37 Among South Auckland
women with gestational diabetes mellitus (GDM), a high proportion (4.3%
European, 21% Māori, 21% Pacific) of Polynesians had permanent diabetes
postnatally.38
Gestational diabetesA review of 1994/95
hospital records in
South Auckland showed high rates of GDM in Māori and Pacific women who
attended oral glucose challenge tests compared with Europeans
21. This study
found that Pacific women were more likely to be screened (68.5%) when compared
with Māori (47.3%) when both have high rates of GDM and Type 2
diabetes.
Risk factors for diabetesThe prevalence of obesity in New Zealand has increased from
9.4% in 1977 to 19.9% in 2003 among males, and from 10.8% to 22.1% among
females.39 Māori
and Pacific people have a particularly high prevalence of obesity,23
physical inactivity,13 insulin resistance,13 and metabolic syndrome27 compared
with Europeans (Table 2).
The association between body composition and central fat
distribution with
risk
of diabetes appears to
be independent of ethnicity40. While Asians appear to have comparatively
lower obesity41, Rush et al42 have found high body fat composition for Asian
Indians compared with Europeans for a given BMI.
ComplicationsTable 3 shows the risk factors for microvascular and
macrovascular disease in the New Zealand studies to date. The poor glycaemic and
lipid control among patients attending the clinic from 1992–9544 appears
to have continued into this century. The Otago register has reported a mean
HbA1c of 7.2% for Type 2 patients; 50.1% had HbA1c result >7% in 1998.45 The
results of the Get
Checked
programme showed that 63% of Europeans, 27% of Māori, and 92% of Pacific
people with diabetes had a free annual check in 2004 (personal communication,
MoH). But the denominators are derived from the MOH forecast estimates and
actual percentage of Pacific
people getting free
checks may be much lower. The 2004 results show poorer metabolic control (HbA1c
> 8%), for Māori (40%) and Pacific people (51%) with compared with
European/Other (23%).
Table 2. Prevalence of risk factors for diabetes and
its complications
*Age standardised.
† European includes Other. **The ATP III criteria for metabolic syndrome were considered to have been met when 3 or more of the following factors were present: waist circumference >102cm for men or >88cm for women, treated hypertension or systolic blood pressure (sBP) ≥130mmHg and/or diastolic blood pressure (dBP) ≥85mmHg as mean of two readings, triglycerides ≥1.7mmol/L, HDL <1.04mmol/L for men or <1.29mmol/L for women, fasting blood glucose (FBG) ≥6.1mmol/L, or diabetes. ‡ Obesity is body mass index (BMI) ≥30 for European/Other/Asian, BMI ≥32 for Māori/Pacific. § Asian includes Other. Table 3. Clinical characteristics of diabetes
patients
Data are mean ± SD
unless otherwise stated; * Transferred from diet/pill to insulin; † Data
are geometric mean.
Diabetes-related mortalityNZHIS mortality data has attributed 3% of deaths in 2000 to
diabetes.55 Difficulties in the coding of diabetes have been recognised for many
years,49 yet continue to be rediscovered56 57 with 45%–55% under-coding
especially among non-insulin using (Type 2) patients.
In spite of inadequate mortality statistics, the
standardised mortality rate for diabetes mellitus during 1999 were 62.5 per
100,000 in Maori versus 11 in non-Maori 58. A 10-year follow-up of the
predominantly European Type 2 diabetic cohort in Canterbury showed increased
mortality (standardised mortality ratio 2.17), the cause of death being
predominantly attributable to cardiovascular disease (CVD) (69.8%).59
The Canterbury insulin-treated Diabetic Registry has
reported a CVD-related standardised mortality ratio of 4.48 for diagnosis age
<30years and 2.05 for diagnosis age ≥30 years among those who commenced
insulin within 12 months of diagnosis.60
The meta-analysis of studies from Asia Pacific region
(including 10,326 subjects from New Zealand) revealed that the hazard ratio
associated with diabetes was significantly higher for fatal cardiovascular
disease (1.97), fatal coronary heart disease (2.19,) and fatal cerebrovascular
disease (2.0).61
Table 4 shows the ethnic specific death rates from ESRD and
ischaemic heart disease in the SADP cohort age 40–79 years.49 The
standardised mortality ratio for renal failure is 8.37%, estimated from the
Canterbury insulin-treated Diabetic Registry.60 This reflects the renal failure
rate in insulin treated diabetes patients in a registry that has predominantly
European patients (97.7%).
Cardiovascular and cerebrovascular diseasesVery few reports relating to heart disease exist (Table 4).
A review of records from Middlemore Hospital has reported significant ethnic
differences in the prevalence of diabetes among in-patients aged 40+ with acute
MI.52
Diabetic nephropathyAmong the 449 new renal disease patients entering the
ANZDATA registry in 2003,54 45% had diabetes (23% of European patients, 65%
Maori, 67% Pacific, 50% Asian).
Diabetic
nephropathy (40%) was the most common cause of end-stage renal disease
(ESRD) in New
Zealand, followed by
glomerulonephritis
(26%) and
hypertension
(10%). Type 2
diabetes (non-insulin and insulin requiring) was identified in 94% of
diabetic nephropathic patients on the registry.
From the prospective data from ANZDATA reports, the numbers
with of diabetes-related ESRD in Maori population are the highest, but appear to
have reached equilibrium (Figure 3).
The incidence of diabetes related ESRD in Europeans while lower than other
ethnic groups, has also doubled since 1992. The crude prevalence of proteinuria
and ESRD were higher in Maori and Pacific people compared with Europeans in the
SADS survey62 in 1990 (Table 4).
Table 4. Diabetes-related mortality and
complications
*Estimated from ANZDATA
Registry 2001 and Census 2001; † Age and sex standardised; ‡ Age
adjusted to total diabetes population; MI=Myocardial infarction.
A familial predisposition to renal disease was suggested
from one study showing that the predisposition to diabetic nephropathy in
Polynesians was associated with a family history of renal disease (rather than a
family history of diabetes), yet associated with diabetes through relative
hypoinsulinaemia and hyperglycaemia.63 Diabetic nephropathy among children and
young adults with Type-1 diabetes was reportedly 19% in the Waikato
area.64
Other diabetes-related complicationsFew studies of diabetic eye and foot disease have been
undertaken. A summary is shown in Table 4. The SADP study in 1992–93 found
significant ethnic differences in the rates of blindness, laser treatment, and
cataract among people with diabetes: Maori and Pacific people having double the
proportions as those of European descent.46
Retinopathy was present in 41% of a Type 2 diabetes cohort
in Canterbury at baseline.59 A decline in the rates of vision-threatening
diabetic retinopathy from 11.5% in 1993 to 1.5% in 2002 has been reported in
diabetes patients in the Waikato area, but Maori had a high
failure-to-attend-screening rate (32.3%) compared with the overall rate of
18.7%.50 Get Checked results for 2004
indicated low eye-screening rates of less than 70% overall, with less than 60%
for Maori and Pacific groups. The rate in those aged under 26 was 13%.64
The prevalence of hospital discharges for diabetic
foot
disease in
New
Zealand
increased from 13.56 in 1980 to 25.79 in 1993.65 The total inpatient cost
for the management of diabetic
foot disease in
New
Zealand
(population 3.3 million) for 1993 was estimated to be in the range of
NZ$10–11 million.
The SADP study found significantly higher numbers of Pacific
peoples with major lesions (amputation or ulcer/blister) compared with European
or Maori diabetes patients (Table 4).51 The Ministry of Health estimated that
Pacific people have more than double rate of lower limb amputation (43.6 per
100,000) in adults aged 25+ compared with the total New Zealand average (17.4)66
in 2004.
The Auckland Leg Ulcer Study in subjects aged 40+ years
showed that 18% of cases had diabetes as a comorbidity whereas only 5.5% of
controls had diabetes.67
ConclusionsWhile the diabetes epidemic continues to impact increasingly
on New Zealanders and its health services during the past 5 years, a growing
number of Government and DHB-funded initiatives are in place to prevent diabetes
and its complications (e.g. Lets Beat Diabetes and Diabetes Projects Trust in
Counties-Manukau, Ngati Porou Hauora Ngatai and Healthy Programme in Taiwawhiti,
Te Whai Matauranga o te Ahua Noho lifestyle program in Otago, and Te Wai o Rona:
Diabetes Prevention Strategy in Waikato/Lakes).
Moreover, several district diabetes registers are in place
or are under development (e.g. in Otago, Canterbury, Waikato and South/West
Auckland), and these are complemented by the
Get Checked data. ANZDATA renal and the
emerging Australasian Diabetes in Pregnancy Society diabetes in pregnancy
registers, along with a several eye screening registers also contribute to our
understanding of diabetes in New Zealand.
The Get Checked
dataset is apparently due to be extended, and this may help provide a more
detailed and comprehensive view of diabetes and its care. Work is now needed on
how best to monitor the incidence and prevalence of diabetes as well as the
proportion of people with undiagnosed diabetes, impaired glucose tolerance, and
impaired fasting glucose. How else will we know that the growing resources
directed towards lifestyle change are having an effect?
To date, the data gathered relating to metabolic control and
complications are patchy, however they suggest that New Zealand needs to do more
to reduce the impact of diabetes on cardiovascular, renal, eye, foot, and
pregnancy related complications. This is particularly the case for Maori and
Pacific peoples, whose metabolic control remains poorer than that for European
New Zealanders.
More aggressive blood pressure, glycaemic, and lipid control
would appear to be needed, and the development of ways to deliver this within
the context of New Zealand (i.e. to its people and its health service) are
urgently required. Such increases in medication use and services (in both
primary and secondary care) are likely to cost more initially and yet little
data exists to guide such development.
PricewaterhouseCoopers Ltd estimated that the Type 2
diabetes cost in 2001 approached NZ$400 million and was predicted a rise to more
than NZ$1000 million by 2021.68 They also estimated that the total cost of
diabetes could be reduced over 20 years if existing services are increased as
soon as possible (by $10 million each year in their enhanced services model).
The models used are not perfect, yet more complete than the earlier Health
Funding Agency report.6 It is surprising that more detailed economic data is not
available.
While there have been a relatively large number of
publications relating to diabetes in New Zealand over the last 5 years, a
significant proportion were from South Auckland in the 1990s and these data are
now ageing. More importantly, while services are developing in primary and
secondary care, evaluation has rarely been sufficiently robust to lead to
publication in peer-reviewed journals. Indeed, funding for such “diabetes
translational research” has been uncommon and fits poorly into the
existing research funding paradigm.
If we are to develop more complex models of care, and
increase access to modern pharmaceuticals and devices, then it is also clear
that we need more research into the impact of such service developments on the
incidence, prevalence, and costs of diabetes and its complications. While this
will not come cheaply, it will be cheaper than the alternative.
A nationally agreed strategic plan is now urgently needed on
how best to monitor and control the increasing incidence and prevalence of
diabetes. In addition, major national surveys are required now to ascertain the
proportion of those people living in New Zealand with impaired fasting glucose
or impaired glucose tolerance, as well as those with undiagnosed diabetes.
Author information:
Grace Joshy, Research Fellow; David Simmons, Professor of Medicine; Waikato
Clinical School, University of Auckland, Hamilton
Acknowledgements: We
acknowledge Professor Ross Lawrenson (Head of Waikato Clinical School,
University of Auckland), Dr Paul Drury (President, NZSSD), Sandy Dawson
(Ministry of Health), and DHB-level diabetes teams for their valuable
input.
Correspondence:
Grace Joshy, Research Fellow in Diabetes Epidemiology, University of Auckland
Waikato Clinical School, Waikato Hospital, Private
Bag 3200, Pembroke Street, Hamilton. Fax: (07) 839 8712; email: joshyg@waikatodhb.govt.nz
References:
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