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Glucose Tolerance and Cardiovascular Mortality
Comparison of Fasting and 2-Hour Diagnostic Criteria
DECODE Study Group; on behalf of the European Diabetes Epidemiology
Group
Arch Intern Med. 2001;161:397-405.
ABSTRACT
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Background New diagnostic criteria for diabetes based on fasting blood glucose
(FBG) level were approved by the American Diabetes Association. The impact
of using FBG only has not been evaluated thoroughly. The fasting and the 2-hour
glucose (2h-BG) criteria were compared with regard to the prediction of mortality.
Methods Existing baseline data on glucose level at fasting and 2 hours after
a 75-g oral glucose tolerance test from 10 prospective European cohort studies
including 15 388 men and 7126 women aged 30 to 89 years, with a median
follow-up of 8.8 years, were analyzed. Hazards ratios for death from all causes,
cardiovascular disease, coronary heart disease, and stroke were estimated.
Results Multivariate Cox regression analyses showed that the inclusion of FBG
did not add significant information on the prediction of 2h-BG alone (P>.10 for various causes), whereas the addition of 2h-BG
to FBG criteria significantly improved the prediction (P<.001 for all causes and P<.005 for
cardiovascular disease). In a model including FBG and 2h-BG simultaneously,
hazards ratios (95% confidence intervals) in subjects with diabetes on 2h-BG
were 1.73 (1.45-2.06) for all causes, 1.40 (1.02-1.92) for cardiovascular
disease, 1.56 (1.03-2.36) for coronary heart disease, and 1.29 (0.66-2.54)
for stroke mortality, compared with the normal 2h-BG group. Compared with
the normal FBG group, the corresponding hazards ratios in subjects with diabetes
on FBG were 1.21 (1.01-1.44), 1.20 (0.88-1.64), 1.09 (0.71-1.67), and 1.64
(0.88-3.07), respectively. The largest number of excess deaths was observed
in subjects who had impaired glucose tolerance but normal FBG levels.
Conclusion The 2h-BG is a better predictor of deaths from all causes and cardiovascular
disease than is FBG.
INTRODUCTION
NEW DIAGNOSTIC criteria for diabetes mellitus based on the fasting blood
glucose level alone (fasting plasma glucose  7.0 mmol/L [126 mg/dL]) were
approved by the American Diabetes Association (ADA) Expert Group.1 For epidemiological purposes, the ADA recommended
the use of fasting glucose level alone and did not recommend the 2-hour 75-g
oral glucose tolerance test. The choice of the cutoff point was based on bimodalities
in the fasting glucose distribution1 and on
the association between fasting glucose level and risk of diabetic retinopathy.
The World Health Organization) adopted the same fasting glucose level as the
ADA, but retained the use of the 2-hour glucose tolerance test for the diagnosis
of diabetes in population studies.2 The 2-hour
75-g oral glucose tolerance test has been the international standard for diabetes
diagnosis since 19853 and the basis of much
epidemiological data in the medical literature about risks of complications
associated with diabetes.
To evaluate the prognostic impact of the new fasting glucose criteria,
the DECODE (Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria
in Europe) Study was initiated. We have previously reported that there was
a high degree of disagreement in the fasting and 2-hour glucose classifications
in European populations.4 Among subjects with
diabetes diagnosed by a fasting glucose level of 7.0 mmol/L or more, only
46% also had 2-hour glucose level of 11.1 mmol/L or more (200 mg/dL),
the 2-hour glucose diagnostic criterion for diabetes.2-3
Furthermore, analyses of the DECODE database showed that abnormalities in
2-hour glucose levels were better predictors of all-cause mortality than fasting
glucose alone.5 A high 2-hour glucose concentration
was found to be associated with an increased risk of death, independent of
the level of fasting blood glucose, whereas mortality associated with the
fasting glucose concentration depended on the level of 2-hour glucose, in
all categories of fasting glucose.
Because most patients with type 2 diabetes mellitus die of cardiovascular
diseases (CVD) and not of microvascular complications, cardiovascular mortality
and morbidity should be considered in defining the diagnostic criteria for
diabetes. Herein we report on cardiovascular deaths as well as all-cause deaths
in the DECODE Study population.
PARTICIPANTS AND METHODS
PARTICIPANTS AND METHODS
The study populations and the methods used to recruit the participants
have been reported previously.4-6
Briefly, researchers in Europe who had performed population-based studies
or large studies in occupational groups using the standard 2-hour 75-g oral
glucose tolerance test were invited to participate in the DECODE Study. Individual
data on fasting and 2-hour glucose concentrations and several other variables
were sent to the Diabetes and Genetic Epidemiology Unit of the National Public
Health Institute in Helsinki, Finland, for collaborative data analyses. In
this article, only the studies with prospective data on cause-specific mortality
and all required confounding variables (cholesterol, blood pressure, smoking
habits, and body mass index) were included.
A total of 13 centers provided cause-specific mortality data for the
DECODE Study, 10 of which provided data with all the covariates required.
All 10 studies included men (n = 15 388) and 6 included women (n = 7126).
Among the 22 514 subjects, aged 30 to 89 years, 796 subjects were previously
diagnosed as having diabetes. For the other 21 718 subjects who had no
previous history of diabetes, the median duration of follow-up was 8.8 years
(5.8 and 20.6 years for the 25th and the 75th quartiles, respectively), and
208 203 person-years in men and 52 536 person-years in women were
accumulated.
Subjects who had not previously been diagnosed as having diabetes were
classified according to the following criteria: (1) 2-hour
glucose criteria alone: 2-hour plasma glucose concentrations of 11.1
mmol/L or more (10.0 mmol/L [180 mg/dL] for whole blood) for diabetes,
7.8 to 11.0 mmol/L (140-198 mg/dL) (6.7-9.9 mmol/L [121-178 mg/dL] for whole
blood) for impaired glucose tolerance (IGT), and less than 7.8 mmol/L (<140
mg/dL) (<6.7 mmol/L [<121 mg/dL] for whole blood) for normal glucose
tolerance; and (2) fasting glucose criteria alone:
fasting plasma glucose level of 7.0 mmol/L or more (126 mg/dL) (6.1
mmol/L [110 mg/dL] for whole blood) for diabetes, 6.1 to 6.9 mmol/L (110-124
mg/dL) (5.6-6.0 mmol/L [101-108 mg/dL] for whole blood) for impaired fasting
glucose (IFG), and less than 6.1 mmol/L (<110 mg/dL) (<5.6 mmol/L [<101
mg/dL] for whole blood) for normal fasting glucose.
Vital status information was recorded for each of the subjects attending
the baseline examination in all of the studies. Subjects who emigrated, for
whom the vital status could not be confirmed, were treated as censored at
the time of emigration. Follow-up was complete, ranging from 95.2% in the
Paris Prospective Study to 100% in most of the other studies.5
Causes of death were classified using the International
Classification of Diseases, Eighth and Ninth Revision, codes 401-448
(CVD), 410-414 (coronary heart disease [CHD]), and 430-438 (stroke).
Body mass index (BMI) was calculated as weight in kilograms divided
by the square of height in meters. Subjects were classified as nonsmokers,
ex-smokers, and current smokers.
STATISTICAL ANALYSIS
Age-standardized mortality was calculated using 10-year age groups,
separately for men and women, and direct standardization for a European standard
population.7 Age- and center-standardized means
were compared using analysis of variance according to the diabetic status
defined by the fasting and by the 2-hour glucose criteria. Hazard ratios of
cause-specific and all-cause mortality were estimated for the various glucose
categories, using the Cox proportional hazards model, and adjusting for age,
center, BMI, systolic blood pressure, serum cholesterol level, smoking status,
and sex if men and women were combined. Results are presented as mortality
hazards ratios and 95% confidence intervals, with respect to the given reference
groups. Cumulative mortality curves were estimated by the same Cox proportional
hazards model. Nested models were compared using a  2 log-likelihood
ratio test to determine whether men and women had significantly different
hazards ratios and whether the fasting glucose criteria or the 2-hour glucose
criteria were independent of each other in predicting mortality from cardiovascular
causes and from all causes. The absolute number of excess deaths from all
cardiovascular causes was calculated by comparison with the group determined
to be strictly normal using both the fasting and the 2-hour glucose criteria.
RESULTS
The number of men and women and the percentage of deaths due to cardiovascular
and all causes, according to the fasting and the 2-hour glucose criteria,
by DECODE study centers, are shown in Table
1and Table 2, respectively,
for subjects not previously known as diabetic. Age-standardized death rates
from all causes and cardiovascular causes were higher in diabetic subjects
than in those not meeting diabetic criteria (Table 1 and Table 2).
Increased mortality was also observed in subjects with IGT (Table 2), whereas there was no difference between subjects with
IFG and those with normal fasting glucose (Table 1). Mortality from the various causes was higher in men than
in women (Table 1 and Table 2).
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Table 1. Number of Subjects and Percentage of Deaths From Cardiovascular
Disease (CVD), Coronary Heart Disease (CHD), Stroke, and All Causes According
to Fasting Glucose Categories, by DECODE Study Centers in Subjects Not Previously
Diagnosed as Diabetic*
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Table 2. Number of Subjects and Percentage of Deaths From Cardiovascular
Disease (CVD), Coronary Heart Disease (CHD), Stroke, and All Causes According
to 2-Hour Glucose Categories, by DECODE Study Centers in Subjects Not Previously
Diagnosed as Diabetic*
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Subjects who had 2-hour glucose levels of 11.1 mmol/L or more (whole
blood, 10.0 mmol/L) and fasting glucose levels less than 7.0 mmol/L (whole
blood, <6.1mmol/L) were older and had higher serum cholesterol levels than
those whose fasting glucose levels were 7.0 mmol/L (whole blood, 6.1
mmol/L) and 2-hour glucose levels less than 11.1 mmol/L (whole blood, <10.0
mmol/L). The latter group was more obese (Table 3).
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Table 3. Characteristics of Diabetic Subjects at Baseline According
to Fasting and 2-Hour Glucose Criteria in Subjects Not Previously Diagnosed
as Diabetic in the DECODE Study*
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Multivariate-adjusted Cox proportional hazards model analyses showed
that diabetic subjects by either the fasting or the 2-hour glucose criteria
had an increased hazards ratio of death from cardiovascular causes and from
all causes compared with those normal on the corresponding criteria (Table 4). The hazards ratios for the various
causes of death tended to be higher in diabetic women than in diabetic men,
but these differences in hazards ratios were significant only for CHD mortality
(2 = 11.57 for fasting glucose criteria and 2
= 11.35 for 2-hour glucose criteria, 3 df, P<.01). Increased hazards ratios for deaths from all-cause,
CVD, and CHD mortality were also observed in subjects with IGT, but not in
subjects with IFG (Table 4). In
a model including the fasting and the 2-hour glucose criteria simultaneously,
the hazards ratios for death from the various causes were only slightly reduced
in individuals with IGT or diabetes for the 2-hour glucose (Table 5), but decreased significantly in subjects with IFG and diabetes
for the fasting glucose. Comparing nested models, inclusion of the fasting
glucose categories did not significantly improve the prediction of the 2-hour
glucose alone, in contrast, addition of the 2-hour categories to the fasting
glucose categories significantly improved the prediction (except in the case
of stroke mortality) (Table 5).
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Table 4. Multivariate-Adjusted Hazards Ratios for Deaths From Cardiovascular
Disease (CVD), Coronary Heart Disease (CHD), Stroke, and All Causes According
to Fasting and 2-Hour Glucose Criteria: The DECODE Study*
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Table 5. Adjusted Hazards Ratios for Deaths From Cardiovascular Disease
(CVD), Coronary Heart Disease (CHD), Stroke, and All Causes With Fasting and
2-Hour Glucose Categories in the Same Model: The DECODE Study*
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The cumulative hazards curves (Figure
1) further illustrate the differences between the 2 diagnostic criteria.
Previously known diabetic subjects had worse survival profiles for fatal CVD
and CHD events than those observed in the newly diagnosed diabetic subjects
according to either the fasting or the 2-hour glucose criteria. The survival
curves for known and screened diabetic subjects were similar for fatal stroke
events and for all-cause mortality. The subjects with IGT had a survival profile
in between the diabetic and the normal subjects according to the 2-hour glucose
criteria and clearly worse than the normal subjects for fatal cardiovascular
events and for all-cause mortality. The subjects with IFG had a survival curve
similar to that of the subjects normoglycemic on the fasting glucose criteria
alone. Overall, the cumulative hazard curves were better separated for the
three 2-hour glucose categories than for the 3 fasting glucose categories,
indicating that the former classification provides a better discrimination
for cardiovascular fatal events and for all-cause death.
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Figure 1. Cumulative hazards curves for
deaths from cardiovascular disease (CVD), coronary heart disease (CHD), stroke,
and all causes, according to fasting and 2-hour glucose criteria. The cumulative
hazards are estimated from Cox proportional hazards models and adjusted for
age, center, sex, body mass index, blood pressure, serum cholesterol levels,
and smoking status. DM indicates diabetes mellitus; IFG, impaired fasting
glucose; and NGT, normal glucose tolerance.
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The highest absolute number of excess cardiovascular deaths attributable
to the fasting and the 2-hour glucose criteria was for subjects with IGT,
particularly those who had normal fasting glucose levels (Figure 2).
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Figure 2. Estimated absolute number of excess
cardiovascular deaths according to the duration of follow-up, with reference
to the fasting and the 2-hour glucose categories in subjects not previously
known as diabetic. Number (n) and the total percentage of subjects in each
glucose category are presented. To convert glucose to milligrams per deciliter,
divide by 0.05551.
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COMMENT
Diabetes is an important independent risk factor for CVD mortality.8-15
Hyperglycemia, in the absence of clinically diagnosed diabetes, has also been
associated with an increased risk of CVD and all-cause mortality in some,
but not all studies.8-11,16-38
The lack of adjustment for the established risk factors, applying unstandardized
methods for the glucose test and the small number of events obtained during
follow-up might have contributed to these inconsistencies. Our analyses, based
on a large European population with more than 260 000 person-years of
follow-up, show that asymptomatic diabetes as well as IGT defined by the 2-hour
glucose criteria alone, increased the risk of death from cardiovascular causes
and all causes, independent of other known risk factors and the level of fasting
glucose. In contrast, mortality associated with the fasting glucose concentration
depended largely on the level of 2-hour glucose.
This study is a collaborative study based on the data collected from
10 different centers in different countries in Europe. There is no uniform
approach to the quality control in the glucose measurements. This was not
possible in such a large collaborative study based on retrospective data.
Also, as in other population studies, fasting status could not always be assured.
It is possible that failure to report prior energy (calorie) consumption resulted
in false elevated fasting glucose concentrations in some individuals, and
these subjects might have been misclassified as diabetic or IFG. However,
the fasting status must also have had an influence on 2-hour glucose values
because fasting and 2-hour glucose concentrations were correlated in subjects
with higher fasting glucose concentrations.3
Moreover, the excess risk of CVD deaths observed among subjects with normal
fasting glucose levels but who were diabetic or IGT according to the 2-hour
glucose criteria could not be explained by the failure to fast.
The fasting glucose concentration has been considered to have good reproducibility,
small variability, and easy application in clinical practice. However, the
fasting state is difficult to assure in a population study,3
and it has been found that fasting glucose level was not more reliable than
postload glucose level when measurements were repeated in an elderly population.39 For epidemiological studies, the ADA did not recommend
the use of the 2-hour glucose measurement.1
However, in our study, the 2-hour glucose value certainly gave additional
prognostic information on the risk of death from various causes. In our study,
about one third of the men (148 of 443) and 44% of the women (94 of 213) who
were diabetic according to the 2-hour glucose criteria were classified as
normal according to the fasting glucose criteria. These subjects carried a
50% higher risk for CVD mortality and 100% higher risk for all-cause mortality
compared with subjects who had strictly normal levels for both glucose criteria.
The fact that inclusion of the 2-hour glucose with the fasting glucose criteria
significantly improved the prediction indicates that the predictive ability
of the fasting glucose largely depended on the levels of 2-hour glucose. Conversely,
that fasting glucose levels did not add statistically significant information
on the prediction of deaths once the 2-hour value was included in the model
demonstrated that the relation between the 2-hour glucose level and the risk
of deaths was independent of the fasting glucose levels.
A new category, IFG, based on fasting glucose level alone was introduced
by the ADA Expert Group.1 It was claimed that
IFG and IGT, based on the 2-hour glucose concentration, were metabolic stages
intermediate between normal glucose homeostasis and diabetes, and both were
risk factors for future diabetes and CVD. It is clear from our study that
people with IFG and IGT do not have a similar prognosis with regard to CVD
risk. We failed to show any independent association of IFG with risk of death
from CVD and CHD; however, IFG was associated with stroke mortality in women.
In contrast, the IGT category based on the 2-hour glucose concentration predicted
mortality from all causes, CVD, and CHD. The largest number of excess CVD
deaths was found in subjects with IGT who had a normal fasting glucose level,
which also indicates that the IGT classification has prognostic importance
and cannot be replaced by IFG.
Diabetic women had a higher hazards ratio of death from the CVD causes
than the diabetic men, although the difference in the hazards ratio between
men and women was statistically significant only for CHD mortality. This finding
was compatible with women's greater relative risk of CVD associated with diabetes,
as reported in other studies.40 In this study,
age-standardized mortality from various causes was higher in men than in women
in each glucose category, especially in the normal glucose category. In men,
the increase in mortality in the normal glucose category reduced the relative
risk of death observed in diabetic men and indicates that men are at higher
risk of death from risk factors other than hyperglycemia.
Age was an important confounding factor. It could be argued that the
excess risk of death in diabetic subjects on the 2-hour glucose criteria could
have been attributed to the older age in this group. However, age has been
adjusted for in the data analyses, and the age difference was too small (only
2 years) to have any serious impact on mortality. Other known CVD risk factors
were also taken into account and are unlikely to have influenced the observed
difference between the fasting and the 2-hour glucose criteria.
In conclusion, diabetes and IGT determined by the 2-hour glucose criteria
predicted mortality from the various causes, independent of the level of fasting
glucose, whereas the association between mortality and diabetes and IFG based
on fasting glucose depended largely on the 2-hour glucose categories. With
regard to the prediction of death, classification by 2-hour glucose concentration
is better than that by fasting glucose.
AUTHOR INFORMATION
Accepted for publication July 20, 2000.
Qing Qiao, MD, PhD, was supported by a fellowship from Novo Nordisk,
Bagsverd, Denmark.
| The DECODE Study Participants
The DECODE Study (Diabetes
Epidemiology:
Collaborative analysis Of Diagnostic Criteria in Europe) was undertaken in 1997 on the initiative of the European Diabetes
Epidemiology Group (chairman: Knut Borch-Johnsen; vice-chairman: Andrew Neil;
secretary: Beverley Balkau).
Investigators and Study Centers (included in this
analysis)
Denmark: Glostrup Population
Studies: Svend Larsen, Knut Borch-Johnsen, Center of Preventive Medicine,
Glostrup; Finland:East-West Finland
Study: Aulikki Nissinen, Juha Pekkanen, Jaakko Tuomilehto, Department
of Epidemiology and Health Promotion, National Public Health Institute, Helsinki; FIN-MONICA (Provinces of Kuopio and North Karelia, Turku, and
Helsinki areas): Jaakko Tuomilehto, Pekka Jousilahti, Jaana Lindstrøm,
Department of Epidemiology and Health Promotion, National Public Health Institute,
Helsinki; Helsinki Policemen Study: Marja Pyörälä,
Kalevi Pyörälä, Department of Medicine, University of Kuopio; France: Paris Prospective Study: Beverley
Balkau, Eveline Eschwege, INSERM U258, Paris; Italy: Cremona Study: Giuseppe Gallus, Maria Paola
Garancini, Institute of Medical Statistics–University of Milan and Epidemiology
Unit, S. Raffaele Institute, Milan; the Netherlands: The Hoorn Study Research Group: Lex M. Bouter, Jacqueline
M. Dekker, Robert J. Heine, G. Nijpels, Coen D. A. Stehouwer, Institute for
Research Extramural Medicine, Vrije Universitet, Amsterdam; The Zutphen Elderly Study: Edith J. M. Feskens, Daan Kromhout, Institute
of Public Health, Bilthoven; Sweden: The Northern Sweden MONICA Study: Markku Peltonen, Department of Medicine,
University of Umeå; Poland: POL-MONICA Study (Krakow): A. Pajak, Department of Clinical Epidemiology
and Population Studies, Institute of Public Health, Collegium Medicum, Jagiellonian
University, Krakow.
Secretariat
Knut Borch-Johnsen, Steno Diabetes
Center, Gentofte, Denmark; Johan Eriksson, Qing Qiao, Jaakko Tuomilehto, Department
of Epidemiology and Health Promotion, National Public Health Institute, Helsinki,
Finland.
Data Analysis
Qing Qiao, Department of Epidemiology
and Health Promotion, National Public Health Institute, Helsinki, Finland;
Beverley Balkau, INSERM U258, Paris, France.
Writing Committee
Qing Qiao, Jaakko Tuomilehto,
Diabetes and Genetic Epidemiology, Department of Epidemiology and Health Promotion,
National Public Health Institute, Helsinki; Beverley Balkau, INSERM U258,
Paris, France; Knut Borch-Johnsen, Steno Diabetes Center, Gentofte, Denmark;
Kalevi Pyörälä, Department of Medicine, University of Kuopio,
Finland.
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Corresponding author and reprints: Qing Qiao, MD, PhD, Diabetes and
Genetic Epidemiology Unit, Department of Epidemiology and Health Promotion,
National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki,
Finland (e-mail: qing.qiao{at}ktl.fi).
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