Context Although the excess prevalence of type 2 diabetes mellitus in African
Americans is well established, few studies have compared incident diabetes
in African American and white persons.
Objectives To compare risk of incident diabetes in African American vs white adults
and to identify explanatory factors for racial disparities.
Design Prospective cohort study using baseline data collected from 1986 to
1989 from the ongoing Atherosclerosis Risk in Communities (ARIC) Study, with
9 years of follow-up.
Setting and Participants A total of 2646 African American and 9461 white adults aged 45 to 64
years without diabetes at baseline, sampled from 4 US communities.
Main Outcome Measures Incident type 2 diabetes, ascertained by self-report of physician diagnosis,
use of diabetes medications, or fasting glucose level of at least 7.0 mmol/L
(126 mg/dL), compared among white and African American subjects and by presence
of potentially modifiable risk factors.
Results Diabetes incidence per 1000 person-years was about 2.4-fold greater
in African American women (25.1 [95% confidence interval {CI}, 22.4-28.1]
vs 10.4 [95% CI, 9.4-11.4]) and about 1.5-fold greater in men (23.4 [95% CI,
19.9-27.2] vs 15.9 [95% CI, 14.6-17.2]) than in their white counterparts (P<.001). Results from proportional hazards regression
models indicated that racial differences in potentially modifiable risk factors,
particularly adiposity, accounted for 47.8% of the excess risk in African
American women but accounted for little excess risk in African American men.
Compared with their white counterparts, African American men and women had
higher blood pressures before diabetes onset (diastolic blood pressure difference=5.6
mm Hg in women and 8.4 mm Hg in men; P=.005).
Conclusions Our data indicate that compared with their white counterparts, middle-aged
African Americans are at greater risk of developing type 2 diabetes and have
higher blood pressure prior to development of diabetes. In women, almost 50%
of this excess risk might be related to potentially modifiable factors.
Diabetes mellitus imposes a major burden on the public health of the
United States, leading annually to more than 300,000 deaths and about $100
billion in total costs.1,2 Approximately
90% of diabetic Americans are classified as having type 2 diabetes.3 Data from studies of nationally representative samples
indicate that, compared with their white counterparts, African American men
are 20% to 50% more likely and African American women more than 100% more
likely to have4 or to develop5,6
diabetes. One possible explanation for this excess risk is racial differences
in the prevalence of established risk factors for type 2 diabetes, such as
adiposity, physical inactivity, low socioeconomic status, and family history
of diabetes.7 The identification of potentially
modifiable risk factors as contributors to excess diabetes risk in African
Americans would suggest possible targets for prevention strategies. Unfortunately,
previous investigations in this area have been limited by cross-sectional
study designs,8-10
samples atypical of the general population,11,12
and lack of data on diabetes-related health behaviors and traits, such as
fasting blood glucose levels.5,6
We conducted a prospective study of a community-based, biracial cohort
of middle-aged adults with the following objectives: to compare the risk of
incident diabetes in African Americans vs whites, to determine the extent
to which excess diabetes risk in African Americans was explained by racial
differences in established diabetes risk factors, and to compare diabetes-related
traits (eg, blood pressure and plasma lipid concentrations) in African Americans
and whites 3 to 9 years before the onset of diabetes. We hypothesized that
an adverse profile of potentially modifiable risk factors in African Americans
would lead to a substantial racial disparity in incident diabetes risk.
The Atherosclerosis Risk in Communities (ARIC) Study is an ongoing,
longitudinal cohort study of atherosclerotic cardiovascular disease in 15,792
adults aged 45 to 64 years at baseline. The cohort was selected by probability
sampling from 4 US communities: Forsyth County, North Carolina; Jackson, Miss;
the northwest suburbs of Minneapolis, Minn; and Washington County, Maryland.
By design, the Jackson, Miss, site exclusively recruited African Americans,
thereby accounting for 90% of African Americans in the study. Most of the
remaining African Americans came from the Forsyth County cohort. The sampling
procedures and methods used in ARIC have been described in detail elsewhere.13 Baseline visits were conducted from 1986 through
1989. Participants were followed up subsequently by annual telephone interviews
and clinic visits every 3 years, for a total of 9 years of follow-up.
To construct the cohort for the present analysis, we excluded individuals
who met any of the following conditions: diabetes mellitus present at baseline
(n=1870); race other than white or African American (n=45); fasted for 8 hours
or less before baseline visit (n=337); had missing baseline data on exposures
or diabetes status (n=393). We also excluded individuals in the upper or lower
1% of dietary energy intake who were presumed to represent outliers (n=237).
After these exclusions, we were left with a cohort of 12,910 of whom 803 (6.2%)
failed to return to the clinic, leaving 12,107 participants with data on incident
diabetes.
Assessment of Baseline Characteristics
Interview and Questionnaires. Information on age, sex, race, educational attainment, and family history
of diabetes was based on self-report. A positive family history of diabetes
was defined by participant report of diabetes in either biological parent.
Parents whose diabetes status could not be recalled were classified as nondiabetic.
Physical activity was assessed using a modified version of the questionnaire
developed by Baecke et al.14 Activity was classified
as either sports-related (eg, jogging) or non–sports-related leisure
activity (eg, gardening) and measured on a 5-point scale, with 1 indicating
the lowest level of activity and 5 the highest. Cigarette use was classified
as never, former, or current. Alcohol consumption was assessed by the question:
"During a typical week, how many glasses of wine/cans of beer/mixed drinks
do you consume?" After pooling across beverage type, individuals were classified
by the number of alcoholic drinks consumed per day. Dietary energy intake
was assessed using an interviewer-administered, modified version of the 61-item
food frequency questionnaire developed by Willett et al.15
Laboratory Evaluation. Participants were asked to fast for at least 12 hours before morning
blood collection. After applying a tourniquet, blood was drawn from the antecubital
vein while participants were seated. Blood specimens were collected into vacuum
tubes containing serum-separator gel (glucose, insulin, creatinine and uric
acid chemistries) and EDTA (lipids). Tubes were centrifuged at 3000g for 10 minutes at 4°C. After separation, aliquots were quickly
frozen at −70°C until analysis was performed (within a few weeks).
Serum glucose was assessed by a modified hexokinase/glucose-6-phosphate dehydrogenase
procedure. Standard radioimmunoassay was used to determine serum insulin level.
Total cholesterol16 and trigylcerides17 were measured by enzymatic methods, high-density
lipoprotein cholesterol was measured after dextran-magnesium precipitation,18 and low-density lipoprotein cholesterol was calculated
using the Friedewald equation.19
Ascertainment of Diabetes Mellitus
Individuals were classified as having diabetes mellitus if any of the
following criteria, adapted from 1997 American Diabetes Association criteria,20 were met: fasting serum glucose levels of at least
7.0 mmol/L (126 mg/dL), nonfasting glucose levels of at least 11.1 mmol/L
(200 mg/dL), current use of medications prescribed to treat diabetes (eg,
insulin or sulfonylureas), or a positive response to the question "Has a doctor
ever told you that you had diabetes (sugar in the blood)?" In this study,
individuals with diabetes at baseline were excluded. Individuals without diabetes
at baseline who subsequently met any of these criteria at visits 2, 3, or
4 were considered to have incident diabetes. All incident cases of diabetes
were classified as type 2, because the age of onset in this middle-aged cohort
was between 45 and 73 years.
Initial analyses focused on potential explanations for the excess risk
of diabetes in African Americans compared with whites. The statistical significance
of baseline differences between African Americans and whites regarding established
and suspected risk factors21,22
for type 2 diabetes was assessed using t tests and χ2 tests. Diabetes incidence rates were determined using a person-years
approach, and a test of proportions was used to assess difference in incident
rates of type 2 diabetes between African Americans and whites. The relative
risks (RRs) of incident diabetes in African Americans vs whites were determined
using proportional hazards models. The base model adjusted for 2 established
nonmodifiable risk factors: age and family history. Subsequent models were
created by introducing groups of potentially modifiable risk factors in sequence.
The extent to which groups of covariates appeared to explain the excess
risk of diabetes in African Americans was characterized by calculating the
percent reduction in RR (PR) associated with adjustment according to the formula,
PR=(ra − rb)/(ra − 1), where
ra is the RR of diabetes in African Americans vs whites in the
base model, adjusted for age and family history; rb is the RR after
additional adjustment for a group of covariates; and ra −
1 is the excess risk of diabetes in African Americans vs whites.23
To assess the robustness of these results, we conducted 2 subsidiary analyses.
First, diabetes was reclassified at baseline and during follow-up using a
fasting glucose level of at least 7.8 mmol/L (140 mg/dL), which corresponds
more closely to 1985 World Health Organization criteria. Second, analyses
were confined to the 3172 participants who resided in Forsyth County, North
Carolina, thereby minimizing the possibility of geographic confounding that
arises from the concentration of African American participants in Jackson,
Miss.
Subsequent analyses focused on biological traits (eg, blood pressure)
that accompany diabetes but which are not known to be causal.24
In these analyses, men and women were stratified by diabetes status during
follow-up, ie, no diabetes throughout follow-up vs diabetes at visits 2, 3,
or 4. t Tests were used to determine the statistical
significance of differences in baseline traits between African Americans and
whites. Analysis of variance was used to test for interaction on an additive
scale between race and diabetes status with regard to each trait.
Risk Factors for Diabetes at Baseline
Table 1 summarizes the presence
of established and suspected risk factors for diabetes at baseline. Apart
from age, the profile of established risk factors for diabetes was clearly
worse in African American women than in their white counterparts. In particular,
African American women had fewer years of formal education, were more likely
to report a family history of diabetes, had greater measures of adiposity
(including body mass index [BMI] and ratio of hip-to-waist circumference),
and reported less physical activity during leisure time. A similar racial
disparity of established diabetes risk factors prevailed in men, with the
notable exception of adiposity, which was similar in African American and
white men.
Other health behaviors hypothesized to influence the risk of diabetes
showed less consistent racial patterns. Compared with their white counterparts,
African American women were less likely to have ever smoked cigarettes, whereas
African American men were equally likely to have ever smoked and more likely
to be smoking currently. Typical consumption of alcoholic beverages was lower
in African American men and women than in whites. Finally, dietary energy
intake was somewhat greater in African American women than in white women,
and somewhat lower in African American men than in white men, but these differences
were not statistically significant.
Incident Type 2 Diabetes Mellitus
During 9 years of follow-up, there were 459 incident cases of diabetes
in African Americans and 966 incident cases in whites, corresponding to substantially
higher sex-specific incidence rates in African Americans than in whites (Table 2). In both absolute and relative
terms, the excess risk of diabetes in African Americans vs whites was greater
in women (absolute risk difference, 14.7 per 1000 person-years; risk ratio=2.41)
than in men (absolute risk difference, 7.5 per 1000 person-years; risk ratio=1.47).
To determine the extent to which the observed excess risk of diabetes
in African Americans might be explained by racial differences in established
and suspected diabetes risk factors at baseline, we constructed a series of
sex-specific proportional hazards models. With adjustment for age and family
history (established, unmodifiable risk factors), African American women were
more than 2½ times more likely to develop diabetes than their white
counterparts (Table 3). These
RRs were attenuated slightly by additional adjustment for education (a marker
of socioeconomic status) and for diabetes-related health behaviors, but more
so by additional adjustment for BMI and ratio of waist-to-hip circumferences.
Thus, racial differences in potentially modifiable risk factors for diabetes,
particularly adiposity, accounted for 47.8% of the excess risk of diabetes
in African American women.
The pattern of adjusted risk was markedly different in men. After adjustment
for age and family history in the base model, the RR of incident diabetes
in African American vs white men was 1.58 (95% confidence interval, 1.32-1.89).
Little or none of this excess risk appeared to be explained by racial differences
in potentially modifiable risk factors: in the final multivariate model, the
RR in African American vs white men was virtually unchanged from the baseline
model (relative risk, 1.62; 95% confidence interval, 1.32-1.99).
These results appeared robust in 2 subsidiary analyses. First, after
reclassification of diabetes using a cutoff of 7.8 mmol/L (140 mg/dL), the
RR of diabetes in African American vs white women was 2.74 in the base model
and 1.86 in the fully adjusted model, indicating 50% excess risk explained;
in contrast, racial differences in established or suspected diabetes risk
factors did not appear to explain any of the excess risk in African American
men (data not shown). Second, an identical pattern of risk was obtained when
the analysis was limited to residents of Forsyth County, North Carolina (data
not shown).
Diabetes-Related Traits at Baseline
We compared diabetes-related biological traits in African Americans
vs whites who went on to develop diabetes during the course of follow-up.
Since these traits were assessed at baseline, they characterize a prediabetic
state, 3 to 9 years before the onset of disease. To provide a context for
these racial comparisons in individuals who did go on to develop diabetes,
we examined the same traits in individuals who did not go on to develop diabetes
throughout follow-up.
Compared with their white counterparts, African American women who subsequently
developed diabetes had higher systolic and diastolic blood pressure, were
more likely to have hypertension, and had higher levels of insulin and high-density
lipoprotein cholesterol but lower concentrations of plasma triglycerides (P for all <.005; Table 4). Other diabetes-related traits—including fasting
levels of glucose, creatinine, uric acid, and low-density lipoprotein cholesterol—were
similar at baseline in African American and white women who would later go
on to develop diabetes. Racial differences in most "diabetes-related" traits
were actually greater in women who did not develop diabetes throughout follow-up.
This was particularly true for blood pressure, hypertension, and serum concentration
of uric acid.
Similar patterns of traits in the prediabetic state were observed in
African American and white men (data not shown). Compared with their white
counterparts, African American men who would go on to develop diabetes had
substantially higher systolic and diastolic blood pressure, were more likely
to have hypertension, and had slightly higher fasting levels of creatinine,
uric acid, and high-density lipoprotein cholesterol, but lower levels of glucose
and triglycerides (P for all <.005). As in women,
these differences were also present in men who did not develop diabetes throughout
follow-up.
Middle-aged African Americans, particularly women, are at substantially
higher risk for incident type 2 diabetes than their white counterparts. An
adverse profile of established diabetes risk factors appears to account for
much of the excess risk in African American women and to a lesser extent in
African American men. Much of this contrast appears to stem from sex differences
in the disparity between African Americans and whites in adiposity, which
was substantial in women but negligible in men. Racial differences in the
prediabetic state largely reflect patterns in the general population of individuals
without diabetes. Compared with their white counterparts, African Americans
who subsequently developed diabetes had higher blood pressure and more hypertension,
but similar (or even more favorable) lipid profiles. Strengths of the ARIC
study that support these conclusions are its prospective design; its large,
population-based sample; and its attention to standardization.
Nonetheless, several possible limitations of the study deserve mention.
The fact that more than 90% of the African American participants were recruited
from a single site (Jackson, Miss) raises the possibility that our results
might be confounded by racial differences in geographic distribution. However,
the similarity of results obtained in a sample of African Americans and whites
from Forsyth County, North Carolina, mitigates this possibility. Treatment
of family history of diabetes as a nonmodifiable (ie, genetic) risk factor
is an oversimplification: shared behaviors and environmental exposures contribute
to familial clustering as well.
Most important, like all racial and ethnic comparisons of disease risk,
it is likely that our results are influenced by residual confounding, especially
regarding socioeconomic status and health behaviors.25
In the United States, race is a complex marker for sociocultural and historical
factors, for which commonly used variables like educational attainment or
self-reported physical activity serve as rough proxies, at best. Therefore,
the residual excess risk of type 2 diabetes in African Americans after multivariate
adjustment should be interpreted cautiously. Likewise, estimates for percentage
of excess risk explained by diabetes risk factors probably represent underestimates.
Since 1965, 8 published studies have investigated the excess risk of
diabetes in African Americans vs whites.5,6,8-12,26
Of these, 4 studied prevalent diabetes using cross-sectional designs8-10,26 and
2 focused on samples atypical of the general population.11,12
Thus, the only previous population-based data regarding incident diabetes
in African Americans vs whites come from the First National Health and Nutrition
Examination Survey (NHANES I) Follow-up Study.5,6
In this nationally representative sample of 1500 African Americans and 9500
whites aged 25 to 70 years, followed up for 16 years, the RR of incident diabetes
for African Americans vs whites was 2.1 among women and 1.6 among men. After
adjustment for age, BMI, ratio of subscapular to triceps skin folds, education,
and physical activity, African Americans remained at higher risk for diabetes
but only at lower levels of adiposity. In men, the RR of diabetes in African
Americans vs whites fell from 1.5 at a BMI of 25 kg/m2 to 1.0 at
a BMI of 30 kg/m2; in women, it fell from 1.6 to 1.3. These results
are generally similar to ours.
In contrast, absolute diabetes incidence rates appeared 2- to 3-fold
higher in men and women of both races in our study than in the NHANES I Epidemiologic
Follow-up Study.5 For example, after accounting
for differences in follow-up time, diabetes incidence (per 1000 person-years)
in African American women aged 45 to 64 years in NHANES I was approximately
11.2 vs 25.1 in our study. A similar disparity was observed when incidence
in whites was compared with previous data from Rancho Bernardo, Calif,27 and San Antonio, Tex.28
Possible explanations for this disparity include differences in age structure,
in regional factors, and in diagnostic criteria. Favoring the latter explanation
is the similarity of results in whites in our study to those observed in a
study of residents of Rochester, Minn,29 with
diagnostic criteria that included a fasting glucose level of at least 6.1
mmol/L (110 mg/dL).
Data from prior studies on racial differences in physiological traits
prior to the onset of diabetes are limited. Like the ARIC Study, the NHANES
I Epidemiologic Follow-up Study demonstrated a racial disparity in systolic
and diastolic blood pressure that was greater in those who remained in a nondiabetic
state throughout follow-up (blood pressure difference between African Americans
vs whites was 7.6 mm Hg vs 5.2 mm Hg in women and 9.1 mm Hg vs 4.9 mm Hg in
men) than in those who subsequently developed diabetes (3.6 mm Hg vs 3.3 mm
Hg in women and 3.1 mm Hg vs 3.1 mm Hg in men, respectively).5,6
In contrast, there was little difference in blood pressure between African
American and white men selected to participate in the Multiple Risk Factor
Intervention Trial, whether or not they developed diabetes.12
That trial also differed from our study regarding racial differences in several
metabolic traits, including levels of fasting glucose, uric acid, and high-density
and low-density lipoprotein cholesterol. However, since the selection process
for the Multiple Risk Factor Intervention Trial was largely based on blood
pressure and plasma lipids, it is likely that these comparisons were influenced
by selection bias.
Growing evidence for a syndrome of insulin resistance as a "common soil"
for both diabetes and vascular disease30 raises
the question of whether differences in such a syndrome between African Americans
and whites31 might explain racial patterns
in diabetes complications. Compared with their white counterparts, African
Americans with diabetes are at much higher risk for end-stage renal disease,
lower extremity amputation, and blindness7—all
strongly related to hyperglycemia and high blood pressure32,33
but weakly related to dyslipidemia. In contrast, the risk of ischemic heart
disease and cardiovascular disease mortality appears similar in both African
Americans and whites with diabetes.1,7
These macrovascular complications are strongly related to dyslipidemia, as
well as to high blood pressure. Therefore, the prediabetic pattern of metabolic
traits observed in our study raises the possibility that preexisting high
blood pressure—but not dyslipidemia or hyperglycemia—in African
Americans who go on to develop diabetes might contribute to their excess risk
of diabetic microvascular complications.
Our study has several implications. It supports the notion that almost
half of the excess risk of type 2 diabetes in African American women might
be attenuated by prevention strategies aimed at weight reduction, dietary
modification, and increased physical activity. It also suggests high blood
pressure in the prediabetic state as a potential target for interventions
designed to reduce the excess risk of microvascular complications in African
Americans with diabetes. Finally, it should stimulate research into novel
risk factors that might contribute to a more complete picture of excess diabetes
risk in African Americans, including susceptibility gene variants34 and adverse environmental exposures in early life.35
1.Geiss L, Herman W, Smith P. Mortality in non–insulin-dependent diabetes. In: National Diabetes Data Group, ed. Diabetes
in America. Bethesda, Md: US Dept of Health and Human Services, Public
Health Service, National Institutes of Health; 1995:233-257.
2.American Diabetes Association. Economic consequences of diabetes mellitus in the U.S. in 1997.
Diabetes Care.1998;21:296-309.Google Scholar 3.Kenny SJ, Aubert RE, Geiss LS. Prevalence and incidence of non–insulin-dependent diabetes. In: National Diabetes Data Group, ed. Diabetes
in America. Bethesda, Md: US Dept of Health and Human Services, Public
Health Service, National Institutes of Health; 1995:47-68.
4.Harris MI, Flegal KM, Cowie CC.
et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose
tolerance in U.S. adults.
Diabetes Care.1998;21:518-524.Google Scholar 5.Lipton RB, Liao Y, Cao G, Cooper RS, McGee D. Determinants of incident non–insulin-dependent diabetes mellitus
among blacks and whites in a national sample: The NHANES I Epidemiologic Follow-up
Study.
Am J Epidemiol.1993;138:826-839. [published correction appears in Am J Epidemiol. 1994;139:964].Google Scholar 6.Resnick HE, Valsania P, Halter JB, Lin X. Differential effects of BMI on diabetes risk among black and white
Americans.
Diabetes Care.1998;21:1828-1835.Google Scholar 7.Tull ES, Roseman JM. Diabetes in African Americans. In: National Diabetes Data Group, ed. Diabetes
in America. Bethesda, Md: US Dept of Health and Human Services, Public
Health Service, National Institutes of Health; 1995:613-630.
8.Cowie CC, Harris MI, Silverman RE, Johnson EW, Rust KF. Effect of multiple risk factors on differences between blacks and whites
in the prevalence of non–insulin-dependent diabetes mellitus in the
United States.
Am J Epidemiol.1993;137:719-732.Google Scholar 9.O'Brien TR, Flanders WD, Decoufle P, Boyle CA, DeStefano F, Teutsch S. Are racial differences in the prevalence of diabetes in adults explained
by differences in obesity?
JAMA.1989;262:1485-1488. [published correction appears in JAMA. 1990;263:1496].Google Scholar 10.Brancati FL, Whelton PK, Kuller LH, Klag MJ. Diabetes mellitus, race, and socioeconomic status: a population-based
study.
Ann Epidemiol.1996;6:67-73.Google Scholar 11.Pavlik VN, Nichaman MZ, Vallbona C. NIDDM incidence in a tri-ethnic population of diagnosed hypertensives.
Ethn Dis.1996;6:213-223.Google Scholar 12.Shaten BJ, Smith GD, Kuller LH, Neaton JD. Risk factors for the development of type II diabetes among men enrolled
in the usual care group of the Multiple Risk Factor Intervention Trial.
Diabetes Care.1993;16:1331-1339.Google Scholar 13.The ARIC Investigators. The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives.
Am J Epidemiol.1989;129:687-702.Google Scholar 14.Baecke JA, Burema J, Frijters JE. A short questionnaire for the measurement of habitual physical activity
in epidemiological studies.
Am J Clin Nutr.1982;36:936-942.Google Scholar 15.Willett WC, Sampson L, Stampfer MJ.
et al. Reproducibility and validity of a semiquantitative food frequency questionnaire.
Am J Epidemiol.1985;122:51-65.Google Scholar 16.Siedel J, Hagele EO, Ziegenhorn J, Wahlefeld AW. Reagent for the enzymatic determination of serum total cholesterol
with improved lipolytic efficiency.
Clin Chem.1983;29:1075-1080.Google Scholar 17.Nagele U, Hagele EO, Sauer G.
et al. Reagent for the enzymatic determination of serum total triglycerides
with improved lipolytic efficiency.
J Clin Chem Clin Biochem.1984;22:165-174.Google Scholar 18.Warnick GR, Benderson JM, Albers JJ. Quantitation of high-density lipoprotein subclasses after separation
by dextran sulfate and Mg2+ precipitation [abstract].
Clin Chem.1982;28:1574.Google Scholar 19.Friedewald WT, Levy RI, Frederickson DS. Estimation of the concentration of low-density lipoprotein cholesterol
in plasma, without the use of preparative ultracentrifuge.
Clin Chem.1972;18:499-502.Google Scholar 20.The Expert Committee on the Diagnosis and Classification of Diabetes
Mellitus. Report of the Expert Committee on the Diagnosis and Classification
of Diabetes Mellitus.
Diabetes Care.1999;22:S5-S19.Google Scholar 21.Holbrook TL, Barrett-Connor E, Wingard DL. A prospective, population-based study of alcohol use and non–insulin-dependent
diabetes mellitus.
Am J Epidemiol.1990;132:902-909.Google Scholar 22.Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC. Prospective study of cigarette smoking, alcohol use, and the risk of
diabetes in men.
BMJ.1995;310:555-559.Google Scholar 23.Breslow NE, Day NE. Statistical Methods in Cancer Research. Lyon, France: International Agency for Research on Cancer, IARC Publications;
1990:76-78. Publication 32.
24.Gress TW, Nieto FJ, Shahar E, Wofford MR, Brancati FL. Hypertension and antihypertensive therapy as risk factors for type
2 diabetes mellitus.
N Engl J Med.2000;342:905-912.Google Scholar 25.Kaufman JS, Cooper RS, McGee DL. Socioeconomic status and health in blacks and whites: the problem of
residual confounding and the resiliency of race.
Epidemiology.1997;8:621-628.Google Scholar 26.Bonham GS, Brock DB. The relationship of diabetes with race, sex, and obesity.
Am J Clin Nutr.1985;41:776-783.Google Scholar 27.McPhillips JB, Barrett-Connor E, Wingard DL. Cardiovascular disease risk factors prior to the diagnosis of impaired
glucose tolerance and non–insulin-dependent diabetes mellitus in a community
of older adults.
Am J Epidemiol.1990;131:443-453.Google Scholar 28.Burke JP, Williams K, Gaskill SP, Hazuda HP, Haffner SM, Stern MP. Rapid rise in the incidence of type 2 diabetes from 1987 to 1996: results
from the San Antonio Heart Study.
Arch Intern Med.1999;159:1450-1456.Google Scholar 29.Melton III LJ, Palumbo PJ, Chu DP. Incidence of diabetes mellitus by clinical type.
Diabetes Care.1983;6:75-86.Google Scholar 30.Stern MP. Do non–insulin-dependent diabetes mellitus and cardiovascular
disease share common antecedents?
Ann Intern Med.1996;124(1 pt 2):110-116.Google Scholar 31.Schmidt MI, Duncan BB, Watson RL, Sharrett AR, Brancati FL, Heiss G.for the Atherosclerosis Risk in Communities Study Investigators. A metabolic syndrome in whites and African-Americans: The Atherosclerosis
Risk in Communities Baseline Study.
Diabetes Care.1996;19:414-418.Google Scholar 32.UK Prospective Diabetes Study Group. Intensive blood glucose control with sulphonylureas or insulin compared
with conventional treatment and risk of complications in patients with type
2 diabetes (UKPDS 33).
Lancet.1998;352:837-853. [published correction appears in Lancet. 1999;354:602].Google Scholar 33.UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular
complications in type 2 diabetes: UKPDS 38.
BMJ.1998;317:703-713. [published correction appears in BMJ. 1999;318:29].Google Scholar 34.Lei HH, Coresh J, Shuldiner AR, Boerwinkle E, Brancati FL. Variants of the insulin receptor substrate-1 and fatty acid binding
protein-2 genes and the risk of type 2 diabetes, obesity, and hyperinsulinemia
in African-Americans: the Atherosclerosis Risk in Communities Study.
Diabetes.1999;48:1868-1872.Google Scholar 35.Hales CN, Barker DJ, Clark PM.
et al. Fetal and infant growth and impaired glucose tolerance at age 64.
BMJ.1991;303:1019-1022.Google Scholar