The Finnish Diabetes Risk Score Is Associated with Insulin Resistance and

Progression towards Type 2 Diabetes

Peter E. H. Schwarz, Jiang Li, Manja Reimann, Alta E. Schutte, Antje Bergmann, Markolf Hanefeld, Stefan R.
Bornstein, Jan Schulze, Jaakko Tuomilehto and Jaana Lindström

J. Clin. Endocrinol. Metab. 2009 94:920-926 originally published online Dec 23, 2008; , doi: 10.1210/jc.2007-2427

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ORIGINAL ARTICLE

E n d o c r i n e C a r e

The Finnish Diabetes Risk Score Is Associated with

Insulin Resistance and Progression towards Type 2
Diabetes

Peter E. H. Schwarz,* Jiang Li,* Manja Reimann, Alta E. Schutte, Antje Bergmann,
Markolf Hanefeld, Stefan R. Bornstein, Jan Schulze, Jaakko Tuomilehto,
and Jaana Lindström
Department of Medicine III (P.E.H.S., J.L., M.R., A.B., S.R.B., J.S.), Medical Faculty Carl Gustav Carus of the Technical
University Dresden, 01307 Dresden, Germany; School for Physiology, Nutrition and Consumer Sciences (A.E.S.) of
North-West University (Potchefstroom Campus), 2520 Potchefstroom, South Africa; Centre for Clinical Studies (M.H.),
GWT-TUD GmbH, 01187 Dresden, Germany; Department of Public Health (J.T., J.L.), University of Helsinki, 00300
Helsinki, Finland; Diabetes Unit (J.L.), Department of Health Promotion and Chronic Disease Prevention, National Public
Health Institute, 00300 Helsinki, Finland; and South Ostrobothnia Central Hospital (J.T.), 60200 Seinäjoki, Finland

Objective: The Finnish Diabetes Risk Score (FINDRISC) questionnaire is a practical screening tool to
estimate the diabetes risk and the probability of asymptomatic type 2 diabetes. In this study we
evaluated the usefulness of the FINDRISC to predict insulin resistance in a population at increased
diabetes risk.

Design: Data of 771 and 526 participants in a cross-sectional survey (1996) and a cohort study
(1997–2000), respectively, were used for the analysis. Data on the FINDRISC and oral glucose tol-
erance test parameters were available from each participant. The predictive value of the FINDRISC
was cross-sectionally evaluated using the area under the curve-receiver operating characteristics
method and by correlation analyses. A validation of the cross-sectional results was performed on
the prospective data from the cohort study.

Results: The FINDRISC was significantly correlated with markers of insulin resistance. The re-
ceiver operating characteristics-area under the curve for the prediction of a homeostasis model
assessment insulin resistance index of more than five was 0.78 in the cross-sectional survey and
0.74 at baseline of the cohort study. Moreover, the FINDRISC at baseline was significantly
associated with disease evolution (P ⬍ 0.01), which was defined as the change of glucose
tolerance during the 3 yr follow-up.

Conclusions: The results indicate that the FINDRISC can be applied to detect insulin resistance in a
population at high risk for type 2 diabetes and predict future impairment of glucose tolerance.
(J Clin Endocrinol Metab 94: 920 –926, 2009)

T he dramatic increase in newly diagnosed cases of type 2 di-

abetes has developed into a major public health concern in
this century (1). Having diabetes means having a significantly
reduced quality of life and reduced life expectancy (2). Further-
more, diabetes and impairment of glucose tolerance are very
common among the elderly (3), and recently also in younger
people, with a most sudden increase in prevalence in the age
group younger than 30 yr (4). An increasing number of people in
their working age are affected by diabetes, increasing the eco-
nomic burden of the health care system due to an earlier onset of
complications, and subsequently, a longer and more intensive
medical treatment period.

ISSN Print 0021-972X ISSN Online 1945-7197
Printed in U.S.A.
Copyright © 2009 by The Endocrine Society
doi: 10.1210/jc.2007-2427 Received November 1, 2007. Accepted December 12, 2008.
First Published Online December 23, 2008
* P.E.H.S. and J.L. contributed equally to this work.
Abbreviations: AUC, Area under the curve; BMI, body mass index; CV, coefficient of
variation; FFA, free fatty acid; FINDRISC, Finnish Diabetes Risk Score; HbA1c, glycosylated
hemoglobin; HDL-c, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model
assessment insulin resistance index; IFG, impaired fasting glucose; IGT, impaired glucose
tolerance; LDL-c, low-density lipoprotein cholesterol; NGT, normal glucose tolerance; NPV,
negative predictive value; OGTT, oral glucose tolerance test; PPV, positive predictive value;
ROC, receiver operating characteristics; TC, total cholesterol.

920 jcem.endojournals.org J Clin Endocrinol Metab. March 2009, 94(3):920 –926

J Clin Endocrinol Metab, March 2009, 94(3):920 –926
Type 2 diabetes is a progressive disease. Before its clinical
onset, there is a long latent asymptomatic period that may last
decades. The development of type 2 diabetes is a multistage pro-
cess originating from genetic disposition (5, 6). Unhealthy life-
style may trigger the development of insulin resistance in a sus-
ceptible genotype (6) that is usually followed by impairment of
glucose tolerance (7). In this prediabetic period, insulin resis-
tance remains often unrecognized because enhanced insulin se-
cretion maintains glucose levels within normal ranges (8, 9).
Owing to the fact that diagnostic criteria for diabetes are based
on the presence of hyperglycemia, this disease is commonly di-
agnosed too late (10, 11). As yet there exist neither diagnostic
criteria for insulin resistance nor suitable screening tools pre-
cluding an early detection of metabolic disturbances. The only
reliable way of assessing insulin resistance is by an euglycemic
clamp, which, unfortunately, is a very costly and time-consum-
ing endeavor to date. The surrogate marker homeostasis model
assessment insulin resistance index (HOMA-IR) established by
Matthews et al. (12) that integrates measures of fasting plasma
glucose and fasting plasma insulin is currently widely used. How-
ever, standardized reference values are lacking. Therefore, there
are attempts to develop simple, fast, and noninvasive scoring
systems for identification of high-risk subjects (13–21). The val-
idated Finnish Diabetes Risk Score (FINDRISC) has been suc-
cessfully implemented as a practical screening tool to assess the
diabetes risk and to detect undiagnosed type 2 diabetes (22, 23).
Beyond this line, it also proved suitable in prediction of coronary
heart disease, stroke, and total mortality in the Caucasian pop-
ulation (24 –27). The present study aimed at evaluating the abil-
ity of the FINDRISC to predict insulin resistance in subjects at
high risk for diabetes mellitus.
Subjects and Methods
Subjects
To address this objective, data of two different samples were ana-
lyzed. The first sample drawn in 1996 consisted of 921 subjects with a
family history of metabolic syndrome. The second sample drawn in 1997
was used for validation purposes and consisted of 735 subjects from
German families with a family history of type 2 diabetes or related insulin
resistance disorders such as obesity or dyslipidemia. The individuals of
both surveys were from the city of Dresden and adjoining areas. Exclu-
sion criteria were previously diagnosed diabetes, severe renal disease,
disease with a strong impact on life expectancy, and therapy with drugs
known to influence glucose tolerance (thiazide diuretics, ␤-blockers, and
steroids). Each subject underwent a physical examination that was fol-
lowed by a 75-g oral glucose tolerance test (OGTT). Blood samples were
taken at fasting, and at 30, 60, 90, and 120 min after the glucose chal-
lenge for measurement of glucose, insulin, proinsulin C peptide, and free
fatty acids (FFAs). In addition, parameters of lipoprotein metabolism [total
cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), and low-
density lipoprotein cholesterol (LDL-c)] were determined from fasting
blood samples. Data on sociodemographical variables, medical history, life-
style, and family history of diabetes were obtained by questionnaires, in-
cluding the FINDRISC questionnaire. A total of 771 and 526 individuals
from the 1996 survey and the 1997 baseline survey, respectively, completed
both the OGTT and the FINDRISC questionnaire.
A follow-up examination was performed 3 yr after the initial survey
in the 1997 cohort. Subjects at an increased diabetes risk based on the
FINDRISC at baseline were either enrolled into a lifestyle intervention or
jcem.endojournals.org 921
underwent pharmacological therapy. The intervention program has been
previously described in detail (28). Of 526 subjects, 515 completed the
follow-up examination. The detailed procedure of the recruitment of
participants and the methods used have been described previously (29,
30). Informed consent was obtained from all participants, and the study
was approved by the local ethics committee.
Analyses
Based on the baseline OGTT data, the subjects were categorized as
having either normal glucose tolerance (NGT), impaired glucose toler-
ance (IGT), including those with impaired fasting glucose (IFG) and type
2 diabetes mellitus according to the World Health Organization/Amer-
ican Diabetes Association criteria of 1997/1999 (31). Subjects with fol-
low-up examination were also defined according to the evolution of their
diabetic status as unchanged, progression, or regression. Estimates for
glucose tolerance were calculated from OGTT parameters. The
HOMA-IR was calculated using the formula as described by Matthews
et al. (12). The area under the curve (AUC) for AUC(insulin), AUC(pro-
insulin), and AUC(FFA) values was estimated from the following equa-
tion (insulin as example):
AUC (insulin) ⫽ 15 ⫻ (“insulin at 0 min” ⫹ 2
⫻ “insulin at 30 min” ⫹ 2 ⫻ “insulin at 60 min” ⫹ 2
⫻ “insulin at 90 min” ⫹ “insulin at 120 min”)
Laboratory procedures
Plasma glucose was measured using the hexokinase method [inter-
assay coefficient of variation (CV) 1.5%]. Serum TC and triglycerides
were determined using enzymatic techniques (Roche Molecular Bio-
chemicals, Mannheim, Germany). HDL-c was determined after precip-
itation with dextran sulfate (Roche Molecular Biochemicals), and serum
LDL-c was calculated using Friedewald’s formula (32). HbA1c values
were analyzed by HPLC. The analyses of insulin and proinsulin levels
were performed by commercially available enzyme immunoassays (Bio-
Source EUROPE S.A Belgium; interassay CV 7.5%, no cross-reactivity
with human proinsulin; DRG Diagnostics, Marburg Germany; interas-
say CV 7.5%, no cross-reactivity with human insulin and C peptide).
FINDRISC
The FINDRISC comprises eight items (22, 25) regarding age, body
mass index (BMI), waist circumference, physical activity, diet, use of
antihypertensive medication, history of high blood glucose, and family
history of diabetes. In the current study, a modified and validated Ger-
man version of the questionnaire was applied (33). In this shortened
version, the variables diet and physical activity were omitted because
both items did not add much power for the prediction of diabetes risk in
previous studies (25). Thus, the maximal achievable score of the modi-
fied questionnaire is 23.
Statistics
Statistical analysis was performed using the Statistical Package for the
Social Sciences (SPSS) software for Windows (version 12.0; SPSS, Inc.,
Chicago, IL). Clinical data are expressed as median and interquartile
range 25%–75%, unless otherwise stated. Individuals with IGT and/or
IFG were analyzed as a combined glucose intolerance group. Associa-
tions and correlation coefficients between the FINDRISC and clinical
parameters were evaluated by the Spearman correlation test. The means
of the FINDRISC total score were compared between the different evo-
lution categories using the Kruskal-Wallis test. A value of P ⬍ 0.05 was
assumed to indicate significance. The predictive value of the modified
FINDRISC (34, 35) for insulin resistance as defined by HOMA-IR value
more than five was evaluated using the AUC in a receiver operating
characteristics (ROC) curve. The sensitivities were plotted against the
y-axis, and the false-positive rates (one-specificity) were plotted against
the x-axis, then the ROC curve was plotted. The optimal cutpoints were
922 Schwarz et al. FINDRISC and Insulin Resistance J Clin Endocrinol Metab, March 2009, 94(3):920 –926

TABLE 1. Selected clinical characteristics of the study participants

1997 survey cohort

Participants at the Participants at the Participants at the
1996 survey baseline survey 3-yr follow-up
No. of men/women 326/445 256/270 250/265
No. of NGT/IFG-IGT/T2D 417/287/67 159/306/61 211/234/70
Age (yr) 43 (30 –57) 59 (51– 63) 62 (54 – 66)
BMI (kg/m2) 25 (22–28) 26 (24 –28) 26 (24 –29)
WHR 0.85 (0.78 – 0.91) 0.89 (0.82– 0.96) 0.88 (0.81– 0.94)
HbA1c (%) 5.2 (4.9 –5.5) 5.6 (5.3– 6.0) 5.4 (5.1–5.8)
FPG (mmol/liter) 5.38 (4.99 –5.85) 5.84 (5.48 – 6.39) 5.61 (5.17– 6.10)
2-h PG (mmol/liter) 6.43 (5.22– 8.02) 6.55 (5.51– 8.20) 6.68 (5.38 – 8.59)
TC (mmol/liter) 5.5 (4.7– 6.3) 5.7 (5.1– 6.4) 5.5 (4.9 – 6.2)
HDL-c (mmol/liter) 1.47 (1.21–1.79) 1.39 (1.14 –1.67) 1.43 (1.18 –1.74)
LDL-c (mmol/liter) 3.32 (2.09 – 4.05) 3.52 (2.91– 4.09) 3.32 (2.76 –3.92)
Fasting insulin (pmol/liter) 62 (43–95) 69 (48 –102) 62 (44 – 89)
2-h insulin (pmol/liter) 279 (178 – 466) 295 (186 –501) 253 (137– 407)
Fasting proinsulin (pmol/liter) 1.81 (1.14 –3.02) 1.85 (1.09 –3.16) 3.51 (2.38 –5.70)
2-h proinsulin (pmol/liter) 11.02 (6.42–17.90) 9.25 (5.89 –16.02) 17.90 (11.26 –27.32)
Fasting FFA (mmol/liter) 0.46 (0.31– 0.62) 0.43 (0.29 – 0.60) 0.54 (0.40 – 0.79)
2-h FFA (mmol/liter) 0.04 (0.03– 0.07) 0.05 (0.03– 0.08) 0.06 (0.04 – 0.10)
HOMA-IR 2.16 (1.42–3.46) 2.62 (1.76 – 4.03) 2.21 (1.54 –3.34)
Data are shown as median (interquartile range). FPG, Fasting plasma glucose; 2-h PG, plasma glucose 2 hr after glucose load; IGT, in which IFG was also included; T2D,
type 2 diabetes; WHR, waist to hip ratio.

located at the peak of the curve where the sum of sensitivity and speci- uals progressed from NGT to IGT/IFG, and 36 previously
ficity is maximal (36). The method of Hanley and McNeil (37) was used healthy persons were diagnosed with manifest diabetes after 3 yr
to compare the AUCs. follow-up. The clinical characteristics of the two study samples
are shown in Table 1.

Results
Of the 326 men and 445 women initially included in the 1996
cross-sectional survey, 417 (54.1%) were diagnosed with NGT,
287 (37.2%) exhibited IGT/IFG, and 67 (8.7%) were newly di-
agnosed with type 2 diabetes. Men had a higher prevalence of
abnormal glucose tolerance than women (51 vs. 42%; P ⫽ 0.012,
␹2 test). Similar proportions were determined in the 1997 cohort
at baseline and after 3 yr follow-up. At baseline, 61 subjects
(11.6%) were newly diagnosed with type 2 diabetes, and 306
(58.2%) individuals had IGT/IFG. The prevalence of impaired
glucose tolerance was 77.3 and 62.6% in men and women, re-
spectively (P ⬍ 0.01). The corresponding values in the follow-up
study were 66.4 and 52.1% (P ⬍ 0.01). In addition, 40 individ-
Association of the FINDRISC and insulin resistance
The mean FINDRISC total score of the 1996 survey was
9.33 ⫾ 5.92 (mean ⫾ SD). The total score ranged from zero to 23
in this group. The individual FINDRISC was evenly distributed
with the majority of subjects ranging between zero and 20. In the
1997 baseline survey, the mean FINDRISC was 7.27 ⫾ 4.45. The
total score ranged from one to 17. The correlation coefficients for
the FINDRISCs and markers of insulin resistance are shown in
Table 2. The FINDRISC was significantly positively associated
with AUC (insulin), AUC (proinsulin), AUC (FFA), HOMA-IR,
and HbA1c in the two baseline surveys. These associations were
still present after 3 yr follow-up. LDL-c was not correlated with
the FINDRISC in the cohort, but a positive association was

TABLE 2. The relationship of the FINDRISC with clinical parameters

1997 survey cohort

1996 survey cohort Baseline 3-yr follow-upa
Coefficients Significance (P value)b Coefficients Significance (P value)b Coefficients Significance (P value)b
AUC (insulin) 0.24 ⬍0.01 0.35 ⬍0.01 0.31 ⬍0.01
AUC (proinsulin) 0.28 ⬍0.01 0.25 ⬍0.01 0.24 ⬍0.01
AUC (FFA) 0.34 ⬍0.01 0.20 ⬍0.01 0.23 ⬍0.01
HOMA-IR 0.42 ⬍0.01 0.45 ⬍0.01 0.46 ⬍0.01
LDL-c 0.34 ⬍0.01 ⫺0.017 0.73 ⫺0.02 0.69
HDL-c ⫺0.07 0.06 ⫺0.17 0.01 ⫺0.21 ⬍0.01
HbA1c 0.39 ⬍0.01 0.29 ⬍0.01 0.21 ⬍0.01
a
The associations are between the FINDRISC of the baseline survey and clinical parameters of the follow-up survey.
b
Spearman correlation test.
J Clin Endocrinol Metab, March 2009, 94(3):920 –926 jcem.endojournals.org 923

HOMA-IR AUC (Insulin) AUC(Proinsulin) AUC(FFA)

20 200000 6000 100

R2=0.10 R2=0.06 R2=0.07 R2=0.11

5000 80
15 150000

4000
60

10 100000 3000

40
1996 study 2000

AUC(P roinsulin)
5 50000

AUC(I nsulin)
20

AUC(FFS)
1000
HOMA

0 0 0 0

0 2 4 6 8 10 12 14 16 18 20 22 0 2 4 6 8 10 12 14 16 18 20 22 0 2 4 6 8 10 12 14 16 18 20 22 0 2 4 6 8 10 12 14 16 18 20 22
1 3 5 7 9 11 13 15 17 19 21 23 1 3 5 7 9 11 13 15 17 19 21 23 1 3 5 7 9 11 13 15 17 19 21 23 1 3 5 7 9 11 13 15 17 19 21 23

Sc ore Sc ore S core Score

20 200000 6000 100

R2=0.14 2
R =0.10 5000
R2=0.06 R2=0.02
16 80
150000

4000
12 60

100000 3000
1997 baseline 8 40

study 2000

AUC(P roins ulin)

50000
AUC(I ns ulin)

4 20

AUC(FFS)
1000
HOMA

0 0 0 0
1 3 5 7 9 11 13 15 17 1 3 5 7 9 11 13 15 17 1 3 5 7 9 11 13 15 17 1 3 5 7 9 11 13 15 17

Sc ore Sc ore S core Score

FIG. 1. Relationship between insulin resistance parameters and FINDRISC (scatter diagrams). The scatter plots illustrate the relationship between FINDRISC and clinical
parameters reflecting insulin resistance. The FINDRISC is depicted on the x-axis of each figure; the clinical parameters are depicted on the y-axis. R2 is the coefficient of
determination for the linear regressions.

found in the 1996 survey. In the same survey, there was a ten- the 256 individuals participating in the follow-up examinations,
dency of an association between HDL-c and FINDRISC (P ⫽ only 10 had an HOMA-IR more than five.
0.06, Spearman test). In contrast, the HDL-c level was signifi-
cantly inversely correlated with the FINDRISC value in the co- Association of the FINDRISC and the evolution of
hort. The relationship between the FINDRISC value and mark- hyperglycemia
ers of insulin resistance is depicted in Fig. 1 (R2 is the coefficient The FINDRISC was significantly directly associated with
of determination for the linear regressions). Accordingly, more disease evolution (P ⬍ 0.01, Kruskal Wallis test). A mean
than 6% of variability in most indicators can be explained by the FINDRISC value found in subjects remaining NGT was 5.32 ⫾
FINDRISC. 3.68 (n ⫽ 116), subjects with disease regression 6.74 ⫾ 3.55 (n ⫽
114), in subjects remaining IGT/IFG 7.54 ⫾ 4.08 (n ⫽ 175),
The predictive performance of the FINDRISC for high
HOMA-IR values
The ROC curves are shown in Fig. 2. The AUC values of 0.78
and 0.74 for the 1996 and 1997 baseline studies, respectively, did
not differ significantly between the two study samples (P ⬎ 0.05).
The optimal cutpoints were 12 and nine, respectively. In the 1996
survey, the sensitivity, specificity, positive predictive value
(PPV), and negative predictive value (NPV) for a FINDRISC
value of 12 or more were 77.5, 67.9, 19.7, and 96.8%, respec-
tively. The corresponding values in the 1997 baseline study for
a FINDRISC value of nine or more were 72.7, 68.2, 29.4, and
88.1%, respectively (Table 3). The relative risk for a FINDRISC
value of 12 or more vs. FINDRISC value less than 12 was 6.04
(95% confidence interval 3.53–10.33) in the 1996 cohort and
2.48 (95% confidence interval 1.58 –3.88) in the 1997 baseline
investigation. Using a HOMA-IR value of two instead of five as
the cutpoint, the ROC-AUC was 0.69 for the 1996 survey and
0.68 for the 1997 baseline study.
If we excluded all individuals whose HOMA-IR was more
than five and all diabetic patients of 1997 baseline study and used
the FINDRISC to predict HOMA-IR (⬎ 5), the relevant ROC-
FIG. 2. ROC curve for the prediction of subjects with HOMA-IR greater than five
AUC was 0.72 (Fig. 2). At the optimal cutpoint of nine, the by the FINDRISC in the 1996 and 1997 baseline studies, as well as in the follow-
sensitivity and specificity were 70.0 and 74.4%, respectively. Of up investigation.
924 Schwarz et al. FINDRISC and Insulin Resistance J Clin Endocrinol Metab, March 2009, 94(3):920 –926

TABLE 3. The sensitivity, specificity, PPV, and NPV by each score in the two surveys

1996 survey 1997 baseline survey

Total score Sensitivity Specificity PPV NPV Sensitivity Specificity PPV NPV
0 1 0 0.092
1 0.972 0.066 0.095 0.959 1 0 0.157
2 0.972 0.097 0.098 0.972 1 0.052 0.164 1.000
3 0.972 0.109 0.100 0.975 0.984 0.141 0.176 0.979
4 0.972 0.221 0.112 0.987 0.967 0.281 0.200 0.979
5 0.958 0.256 0.115 0.984 0.951 0.346 0.213 0.974
6 0.930 0.354 0.127 0.980 0.885 0.388 0.212 0.948
7 0.901 0.420 0.136 0.977 0.852 0.483 0.235 0.946
8 0.873 0.454 0.139 0.972 0.803 0.578 0.262 0.940
9 0.845 0.516 0.150 0.970 0.721 0.682 0.297 0.929
10 0.831 0.573 0.165 0.971 0.557 0.737 0.283 0.899
11 0.817 0.633 0.184 0.972 0.443 0.804 0.296 0.886
12 0.775 0.679 0.197 0.968 0.41 0.817 0.294 0.881
13 0.704 0.741 0.216 0.961 0.377 0.838 0.302 0.878
14 0.662 0.787 0.239 0.958 0.361 0.869 0.339 0.880
15 0.535 0.825 0.236 0.946 0.262 0.92 0.379 0.870
16 0.451 0.860 0.246 0.939 0.164 0.96 0.433 0.860
17 0.423 0.893 0.286 0.939 0.098 0.976 0.432 0.853
18 0.380 0.911 0.302 0.935
19 0.310 0.936 0.329 0.930
20 0.268 0.951 0.357 0.928
21 0.183 0.977 0.446 0.922
22 0.127 0.990 0.563 0.918
23 0.028 0.996 0.415 0.910
Values in bold represent the best cut-points.

subjects with disease progression 8.49 ⫾ 5.24 (n ⫽ 76), and
subjects remaining diabetic 10.68 ⫾ 4.10 (n ⫽ 34). Subjects with
the highest FINDRISC value had the highest proportion of in-
dividuals with diabetes at baseline, and the largest proportion of
them remained diabetic during the follow-up, whereas those
with a low FINDRISC value comprised the highest proportion of
individuals remaining NGT.
Discussion
The data presented in this investigation provide evidence that the
FINDRISC is significantly associated with markers of insulin
resistance and with disease evolution. Because insulin resistance
always precedes IGT (7), the FINDRISC may be a useful instru-
ment to identify people at the earliest stage of disease develop-
ment. Compared with the elaborate and expensive standard pro-
cedure using biochemistry, the FINDRISC questionnaire
represents a simple and cost-efficient tool with a good predictive
value to detect undiagnosed diabetes, which can be used in large-
scale studies and even on a care level (25). In addition, we now
show that the FINDRISC is also able to reliably predict insulin
resistance.
The FINDRISC was significantly associated with an unfavor-
able progression of glycemic parameters. These associations
were validated against an independent data set. The results ob-
tained were consistent with those of the original analysis, pro-
viding a strong argument for the robustness of our findings. The
ability of the FINDRISC to detect insulin resistance was similar
to that to predict the development of type 2 diabetes, and better
than to detect previously undiagnosed diabetes (27). This is in
keeping with the fact that insulin resistance precedes the devel-
opment of diabetes (38, 39). Therefore, the FINDRISC may
rather be applied to predict future diabetes than being used for
diabetes diagnosis (25–27). Our cutoff value for HOMA-IR was
based on the general assumption that a value between 2.5 and
five indicates a moderate risk, and a value greater than five is
indicative for a high risk for insulin resistance (34, 35). Because
the AUC values of ROC curves for a cutoff of “5” were greater
than 0.70, it seems that the FINDRISC can be actually used as a
predictive tool for insulin resistance. The most relevant applica-
tion field of FINDRISC is on the primary care level, where pop-
ulation-based screening strategies are needed and widely imple-
mented. The use by primary care physicians or other health care
professionals would facilitate the detection of high-risk subjects
and the institution of early preventive measures. The association
of the FINDRISC with measures of insulin resistance makes the
application of the FINDRISC more relevant and the clinical rel-
evance stronger.
Some limitations of our study warrant consideration. One
could argue that the analysis of only six risk items in the
FINDRISC questionnaire is not reliable because the two ex-
cluded variables, diet and physical activity, have an evidenced
impact on diabetes development (40 – 42). It could be shown
in two independent studies using the FINDRISC that these two
items did not add much power to the prediction of diabetes
risk (25, 43). Other studies also reported similar observations
(44, 45). The developers of the FINDRISC justified the inclu-
sion of these items, owing to its relevance for the development
of diabetes, particularly because the FINDRISC (and other
J Clin Endocrinol Metab, March 2009, 94(3):920 –926
similar tools) is primarily targeted to laymen or to be used in
the context of diabetes prevention. Although the FINDRISC
has not been tested in all ethnic groups, it may be widely
applicable because it focuses on general risk factors for type
2 diabetes, which are globally prevalent. An adjustment of
cutpoints and relative weight of some items may be needed in
certain population groups.
The second limitation of our study is that all subjects of the
two cohorts had high risks for type 2 diabetes mellitus, thus, the
selection bias may lead to an underestimation of associations.
The mean BMI showed that the 1996 and 1997-baseline samples
were “overweight,” corresponding to 25 (22–28) and 26 kg/m2
(24 –28), respectively. We found that to discriminate high
HOMA-IR values (more than two or more than five) in the 1996
survey and 1997 baseline survey, the performance (ROC-AUC)
of the FINDRISC was similar to that of continuous BMI (data
not shown). However, the benefits of completing a questionnaire
compared with a single BMI measure is a possible increase in
awareness regarding individual risk factors. Therefore, it is nec-
essary to validate the association of FINDRISC and insulin re-
sistance in a randomized study and also in other populations.
Moreover, there were large differences of HOMA in 1996 and
1997 baseline survey (mean ⫾ SD were 0.34 ⫾ 0.28 and 0.43 ⫾
0.28, respectively, data were transformed in log), which could
influence the accuracy of studies too.
Another important aspect is that all individuals at increased
diabetes risk or hyperglycemia at the 1997 baseline survey had
received relevant intervention or treatment in the following
years. This might explain the higher hyperglycemia prevalence at
baseline than after the 3 yr follow-up in this study sample.
Among all these intervened individuals, more than 60% pre-
sented reduced HOMA-IR values at outcome, which could result
in an underestimated incidence of insulin resistance and an un-
derestimated predictive performance of FINDRISC in the pro-
spective analysis. Furthermore, the FINDRISC was correlated
with HOMA-IR at the follow-up, both in those who gained
weight and those with unchanged/reduced body weight as well as
after adjustment for weight change.
In the present analysis, we did not pool the data of the two
samples due to different recruitment procedures. Despite the
small sample sizes, the overall results of both study groups sup-
ported each other. Therefore, the strength of our study is that the
cross-sectional results were validated in an independent cohort.
In conclusion, our analysis shows that the FINDRISC may be
a suitable tool to identify people with insulin resistance, and also
those who are likely to progress toward hyperglycemia and type
2 diabetes.
When implemented in primary health care, the FINDRISC
would assist health care professionals in decision making regard-
ing a further medical investigation and the institution of preven-
tive measures. Furthermore, the application of the FINDRISC in
a population-based program aims also at a learning effect. People
completing the FINDRISC become aware of their own prevalent
risk factors.
Importantly, several authorities such as the European Asso-
ciation for the Study of Diabetes, the European Society of Car-
diology, and the International Diabetes Federation Consensus
jcem.endojournals.org 925
Group have recommended the FINDRISC to be used for risk
stratification purposes in the European population (46, 47).
Acknowledgments
We thank all the patients who cooperated in this study and their referring
physicians and diabetologists in Saxony.
Address all correspondence and requests for reprints to: Peter E. H.
Schwarz, Medical Faculty Carl-Gustav-Carus of the Technical University
Dresden, Medical Clinic III, Building 10, Room 108, Fetscherstrasse 74,
01309 Dresden, Germany. E-mail: peter.schwarz@uniklinikum-dresden.de.
This study was supported by the Commission of the European Com-
munities, Directorate C-Public Health and Risk Assessment, Health &
Consumer Protection, Grant Agreement no. 2004310 with the Project
“DE-PLAN” and by the Dresden University of Technology Funding
Grant, Med Drive.
Disclosure Information: The authors have nothing to declare.
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