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Overweight and Obesity as Determinants of Cardiovascular Risk
The Framingham Experience
Peter W. F. Wilson, MD;
Ralph B. D'Agostino, PhD;
Lisa Sullivan, PhD;
Helen Parise, PhD;
William B. Kannel, MD
Arch Intern Med. 2002;162:1867-1872.
ABSTRACT
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Background To our knowledge, no single investigation concerning the long-term effects
of overweight status on the risk for hypertension, hypercholesterolemia, diabetes
mellitus, and cardiovascular sequelae has been reported.
Methods Relations between categories of body mass index (BMI), cardiovascular
disease risk factors, and vascular disease end points were examined prospectively
in Framingham Heart Study participants aged 35 to 75 years, who were followed
up to 44 years. The primary outcome was new cardiovascular disease, which
included angina pectoris, myocardial infarction, coronary heart disease, or
stroke. Analyses compared overweight (BMI [calculated as weight in kilograms
divided by the square of height in meters], 25.0-29.9) and obese persons (BMI  30)
to a referent group of normal-weight persons (BMI, 18.5-24.9).
Results The age-adjusted relative risk (RR) for new hypertension was highly
associated with overweight status (men: RR, 1.46; women: RR, 1.75). New hypercholesterolemia
and diabetes mellitus were less highly associated with excess adiposity. The
age-adjusted RR (confidence interval [CI]) for cardiovascular disease was
increased among those who were overweight (men: 1.21 [1.05-1.40]; women: 1.20
[1.03-1.41]) and the obese (men: 1.46 [1.20-1.77]; women: 1.64 [1.37-1.98]).
High population attributable risks were related to excess weight (BMI 25)
for the outcomes hypertension (26% men; 28% women), angina pectoris (26% men;
22% women), and coronary heart disease (23% men; 15% women).
Conclusions The overweight category is associated with increased relative and population
attributable risk for hypertension and cardiovascular sequelae. Interventions
to reduce adiposity and avoid excess weight may have large effects on the
development of risk factors and cardiovascular disease at an individual and
population level.
INTRODUCTION
OBESITY COEXISTS with a variety of cardiovascular risk factors and has
been related to greater cardiovascular risk in a variety of observational
studies.1-2 Less well studied
is the relation between categories of adiposity, the development of metabolic
risk factors, and cardiovascular sequelae in a population setting, focusing
on individuals with average weight for height.2-3
Such an approach requires data with repeated measures of weight, risk factor
status, and cardiovascular disease (CVD) incidence. The long-term experience
of the Framingham Heart Study cohort met these requirements and included up
to 44 years of follow-up to study the relation between body mass index (BMI)
and the development of CVD and intervening risk factors in middle-aged men
and women.
Although some investigations have focused on extreme levels of obesity
and their sequelae, the Framingham Heart Study experience represents a community-based
population sample. This setting provided the opportunity to estimate the relative
risks (RRs) and the population attributable risk percentage associated with
adiposity. Earlier research has emphasized the health risks of obesity and
analyzed the effects of variables across a continuum, using relative weights,
skin folds, waist girths, or other measures of adiposity as the factors under
study.4-5 A reliable referent
weight has been missing from such an approach, and reference standards have
been moving targets6 as criteria have changed
over time.7 We strike a medium stance, using
"normal" levels of weight now recommended by obesity experts, a category that
includes about 20% of the population.8 With
the recently adopted broad reference standard of normal weight (BMI [calculated
as weight in kilograms divided by the square of height in meters], 18.5-24.9)
it is likely the RRs of the health hazards we report can be extended to other
population groups. There are constraints with this approach, and what to do
with underweight persons (BMI <18.5) is problematic. We elected to exclude
them because previous experience has shown that this category was likely to
include heavy cigarette consumers, those with severe chronic diseases, and
persons with malignancies.9-12
Our observations spanned several decades from 1948 onward and focused
on multiple measures of BMI. Unfortunately, abdominal girth, triglyceride
and lipoprotein cholesterol levels, and other variables now commonly used
in vascular risk assessment were not determined at these 2-year intervals.
Age was taken into account in bivariate statistical models and included in
all of the multivariable models, and in some instances age categories were
used to investigate the development of risk factors.
PARTICIPANTS AND METHODS
Members of the original Framingham cohort were eligible for the present
study, and the original population sample included 5209 participants aged
30 to 62 years at the initial examination in 1948-1951. We used the technique
of pooled repeated measures,13 an approach
that allowed individuals to contribute multiple person examinations to the
analysis as long as they met the inclusion criteria at the beginning of each
observation interval. Specifically, persons free of CVD at an examination
and with a BMI of 18.5 or greater were eligible for the next period of observation.9-12 Weight,
blood pressure, serum cholesterol, cigarette smoking in the previous year,
menopausal status in women, and interim medication use were ascertained for
each participant at each biennial clinic examination.
Weight was determined to the nearest pound on a physician's scale. Stature,
measured to the nearest quarter inch at the initial Framingham Heart Study
examination, was used. Height and weight were converted to meters and kilograms,
allowing the calculation of BMI for participants at each examination. The
BMI categories (overweight: BMI, 25.0-29.9; obese: BMI 30; normal: BMI,
18.5-24.9) were used in the statistical analyses.8
Individuals with an arterial pressure of 140/90 mm Hg or higher or taking
hypertensive medication were classified as hypertensive. Persons with a casual
blood glucose level of 200 mg/dL (11.1 mmol/L) or greater at the clinic examination,
receiving oral hypoglycemic therapy, or taking insulin were categorized as
having diabetes mellitus, using American Diabetes Association 1997 criteria.14 For the present investigation, hypercholesterolemia
was defined as a clinic blood cholesterol level of 240 mg/dL (6.2 mmol/L)
or greater or reported use of lipid-lowering therapy since the last clinic
examination.15-16 Women who reported
no menstrual periods during the 12 months prior to a clinic examination were
considered menopausal from that time forward. Data from subsequent examinations
were used to reclassify subjects according to their current age, BMI, diabetes
mellitus status, serum cholesterol level, cigarette smoking, and hypertension
status.
Participants were monitored over 2 years after each examination for
the occurrence of an initial CVD event, and participants were followed up
to 44 years for changes in risk factor status. The coronary heart disease
(CHD) end points considered were angina pectoris, myocardial infarction, and
coronary death. Myocardial infarction and coronary death were grouped together
as "hard CHD," and the initial occurrence of any of the 3 CHD end points was
labeled "total CHD." Cerebrovascular disease included the occurrence of new
strokes and transient ischemic attacks, and the end point total CVD was used
for persons who developed either CHD or cerebrovascular disease. The end points
for cardiovascular and cerebrovascular disease were adjudicated by senior
Framingham Study scientists during follow-up, and the diagnostic criteria
for the clinical events have been published elsewhere.17
Age-specific incidence rates for the first occurrence of hypertension,
hypercholesterolemia, diabetes, myocardial infarction, angina pectoris, cerebrovascular
disease, total CHD, and total CVD were calculated according to the most recently
determined BMI category. Analyses were age-adjusted and multivariable adjusted,
including the variables age, hypertension, hypercholesterolemia, and cigarette
smoking. Adjustment for menopausal status was also included for women in multivariable
analyses.
The  coefficients in the pooled logistic regression analyses were
exponentiated to estimate the RR. The SE of the coefficients was used
to calculate the 95% confidence intervals (CIs) of the RR estimates using
published methods.18 Population attributable
risk (PAR) was calculated from the category-specific RR estimate and the prevalence
of the factor using the following equation:
PAR = Proportion of Cases Exposed to the Factor x 100 x (RR - 1)/RR.19-20
When the RR estimate was less than 1.0, the PAR estimate was negative,
representing a potentially preventive effect.19-21
The PAR values for the overweight and obese categories were added together
to estimate the effects of a composite overweight category on risk factor
development and the occurrence of CVD.
RESULTS
Characteristics of the participants are given in Table 1 for men and women according to categories of BMI. The person-years
of experience (bottom row of Table 1)
reflect the cross-sectional pooling of the data over the 44 years of follow-up.
The age entries within the columns give the percentage distribution of the
follow-up experience within a given BMI category. For instance, men aged 56
to 65 years comprised 29% of data experience for the 18.5 to 24.9 BMI category.
The prevalences of risk factors at entry into the study are shown to generally
increase with age. The proportions with elevated cholesterol levels (>240
mg/dL [6.2 mmol/L]) and cigarette use reflect the higher mean cholesterol
levels and a greater proportion of the population smoking in the late 1940s
and early 1950s.
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Table 1. Characteristics of Participants*
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The development of new risk factors and incidence of new events are
given in Table 2 for men and women
according to BMI category. The highest incidence rates consistently observed
were for the development of hypertension, hypercholesterolemia, and the aggregate
development of any of the risk factors (top row of Table 2). The RRs for the new development of risk factors according
to BMI category appear in Table 3.
Age- and multivariable-adjusted estimates are provided, accompanied by the
95% estimates of the RR (Table 3). For instance, the multivariable-adjusted risk of new hypertension in men with
a BMI of 30 or greater was 2.23, and the 95% CI for this estimate was 1.75
to 2.84. The proportion of new hypertension attributable to the obesity category
was 8% in men. As the BMI categories were mutually exclusive, the PAR estimates
could be added together, and the overall effect of overweight or obesity categories
on new hypertension (composite PAR) was 26% (18% + 8%) in men and 28% (17%
+ 11%) in women. Similarly, the RRs and PAR estimates for the occurrence of
hypercholesterolemia (composite PAR, 10% in men and 9% in women) and diabetes
mellitus (composite PAR, 21% in men and 3% in women) are given in Table 3.
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Table 2. Incidence of Risk Factors and Events*
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Table 3. Relative Risk and Population Attributable Risk Percentage
for Adiposity Categories and Risk Factor Development*
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The RRs for new vascular disease events and mortality are presented
in Table 4 and Table 5 for men and women, respectively. These tables duplicate
the format of Table 3. Excess
adiposity was generally associated with a significantly increased RR for cardiovascular
events in men, but no greater risks for myocardial infarction or CVD death
were observed. Relative risks for vascular events associated with overweight
and obesity were often lower in women. The composite PAR estimates for a BMI
of 25 or greater and total CVD (obtained by adding the PAR estimates for overweight
and obesity) were 15% in men and 10% in women. Similarly, the composite PAR
estimates for a BMI of 25 or greater and angina pectoris were 26% in men and
22% in women.
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Table 4. Relative Risk and Population Attributable Risk Percentage
for Adiposity Categories and Vascular Disease Outcomes for Men*
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Table 5. Relative Risk and Population Attributable Risk Percentage
for Adiposity Categories and Vascular Disease Outcomes for Women*
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The PAR percentage estimates from Table 3 through Table 5
are shown in Figure 1 for men and
women. This display generally shows that the PAR levels for the risk factors
and CVD end points are generally similar in women and men, except for hypertension,
which was much greater in women. In addition, the relative contribution of
the overweight category to the occurrence of risk factor development typically
equals the contribution made by the obesity category. This tendency holds
for risk factors and CVD events in both sexes, with a few exceptions, except
for the more serious events among women, in whom the effect of obesity was
much greater than the effect of overweight. In a few instances, the PAR estimates
were negative for overweight (BMI, 25.0-29.9) women, indicative of a protective
effect. With the exception of CVD death in women, these effects were generally
mild and not statistically significant, and the pertinent RRs are given in Table 5.
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Population attributable risk percentage effects for overweight and
obesity on cardiovascular disease (CVD) risk factors and events in Framingham
men and women followed up for 44 years. BMI indicates body mass index; CHD,
coronary heart disease.
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COMMENT
This investigation concerning overweight, obesity, and its cardiovascular
sequelae differs from previous reports in that it focuses on the incidence
of vascular risk factors and CVD sequelae according to specified categories
of adiposity that have been promulgated by American and international expert
panels.8 Our analysis eliminated several features
that may have affected reporting in the past. We adjusted for cigarette smoking,
hypertension, and diabetes mellitus and excluded persons with subnormal levels
of BMI.12 Cross-sectional pooling methods were
used, affecting interpretation of the findings. This analytic technique reassessed
the population every 2 years, and the findings reflect the effects of adiposity
evaluated close to the time that new risk factors or vascular disease outcomes
developed.
Both the overweight and obesity categories were highly related to the
risk of hypertension in men and women. The RR ranged from 1.5 to 1.7 for overweight
and 2.2 to 2.6 for obese persons. The corresponding composite PAR estimates
were greatly increased, and a BMI of 25 or greater accounted for approximately
34% of hypertension in men and 62% of hypertension in women. Other factors,
especially excessive alcohol consumption and estrogen use in women, have been
shown to increase the risk of hypertension, but the population impact is smaller
because the prevalence of each of those factors is lower.22-23
Greater intake of sodium and lower consumption of potassium and calcium have
also been linked to the occurrence of hypertension,24-28
but we did not have serial dietary information to investigate the role of
these cations.
Previous research in the second-generation Framingham Heart Study Offspring
cohort has shown that a variety of factors, including relative weight, heart
rate, alcohol intake, and levels of hematocrit, blood glucose, serum protein,
triglyceride, and phosphorus, were related to hypertension occurrence in one
or both sexes. Excess adiposity has loomed as the most controllable antecedent
factor.29 Clustering of traditional cardiovascular
risk factors has been reported in obese or hypertensive individuals, and the
average number of metabolic abnormalities has been shown to rise monotonically
in proportion to the degree of adiposity.30
Different relations were obtained between adiposity and new hypercholesterolemia.
First, cholesterol levels of 240 mg/dL (6.2 mmol/L) or higher were more common
at the outset of the study, and levels have declined over the past few decades.31 Second, total cholesterol levels tend to increase
between ages 20 and 60 years, and the low-density and very low-density lipoprotein
cholesterol fractions rise, while the high-density lipoprotein cholesterol
fractions remain stable or decline slightly.32
Unfortunately, serial measurements for the lipoprotein fractions were not
available over the course of this investigation. During follow-up, the overweight
participants (but not those who were obese) experienced an increased risk
for new hypercholesterolemia (Table 3).
The nonsignificant result in the obese individuals may be partly attributable
to a greater prevalence of elevated cholesterol level in the obese group at
baseline. In contrast to the findings for hypertension, only 10% of elevated
cholesterol in men and 9% of elevated cholesterol in women was attributable
to overweight and obesity (Table 3).
Previously published cross-sectional studies have shown that greater levels
of BMI are generally associated with greater cholesterol and triglyceride
levels, reduced high-density lipoprotein cholesterol, and smaller low-density
lipoprotein particles.33-34
The incidence of new diabetes mellitus was increased in overweight men
and obese persons of both sexes. No tendency toward an increased risk for
diabetes mellitus was observed for "overweight" women, suggesting that hormonal
factors may play a role. By our analysis, approximately 21% of diabetes in
men was attributable to overweight and obesity, and in women only 3% of diabetes
was attributable to excess adiposity. The findings are highly plausible in
men, but there is no ready explanation for the weaker relations in women.
A variety of issues should be considered. First, it is possible that BMI did
not adequately characterize corpulence and that regional adiposity measures
such as abdominal girth would have classified women better and improved the
prediction.35 Second, the prediabetic state
is often catabolic, and weight loss may have occurred prior to the diagnosis
of type 2 diabetes mellitus. That explanation still would not account for
the sex difference in RRs. Third, age, lipoprotein cholesterol fractions,
inflammatory markers, and hemostatic factors may have played a greater role
in women.36 We did not have information on
these other factors for this study.37 Finally,
our analytic approach examined effects over 2-year intervals. Most cases of
new diabetes mellitus in this population sample occurred after age 65 years,
well past the occurrence of peak weight that has typically been observed between
ages 50 and 60 years.11, 38
Cardiovascular outcomes were highly associated with adiposity, as shown
in Table 4 and Table 5 for men and women, respectively. Framingham obesity and
CVD results have been presented in different forms over the years, including
units of relative weight and percentiles of obesity, but not with the design
to gauge the impact with attributable risk estimates and modern categories
of adiposity. Our data showed that total CHD in men was highly associated
with overweight and obesity, and the RR was stronger for the obesity category.
Of note, however, is that the PAR estimate for total CHD was greater for the
overweight category than for the obese category. This result cannot easily
be attributed to a greater prevalence of overweight in men than in women (Table 1). Perhaps gonadal hormones, other
male and female differences, or factors not available for this analysis were
responsible for this effect. On the other hand, overweight and obesity appeared
to exert similar effects on total CHD risk in women. The RR for total CHD
was of borderline significance in overweight women, but was highly significant
in obese women. The results for total CVD generally paralleled what was observed
for CHD in both sexes across the overweight and obese categories. In this
instance, however, all associations were statistically significant, and the
composite PAR estimates for total CVD were 16% for men and 17% for women.
The adiposity categories tended to have different effects on the various
cardiovascular outcomes in men and women (Table 4 and Table 5).
The end points most highly associated with overweight and obesity among men
were angina pectoris (composite PAR, 26%) and total CHD (composite PAR, 23%).
Negligible effects were observed for CVD death. Similarly, among women, angina
pectoris (composite PAR, 22%) and total CHD (composite PAR, 15%) were highly
associated with overweight and obesity. As the analytic method undertook reappraisal
of events and risk factors at 2-year intervals, only participants free of
CVD were included in subsequent follow-up intervals. Outcomes that were not
first cardiovascular events, such as cerebrovascular disease and cardiac death
that typically occur in older persons, would not be expected to be highly
associated with adiposity under these circumstances.
The findings we reported differ from those reported by others who have
asserted that "overweight is not consistently associated with coronary heart
disease risk."39 Our data merit attention,
as they tend to contravene the preceding statement. In the Framingham experience,
overweight and obesity were highly related to incident hypertension, diabetes
mellitus, and angina pectoris. Among overweight persons, RRs were slightly
stronger in men, but among the obese the RRs were often greater in women.
Past age 50 years, overweight and obesity were very common in women, and this
tendency toward greater adiposity, combined with moderately increased RRs
that accompany the condition, led to impressive PAR estimates for the development
of CVD risk factors and events (Table 3, Table 4, Table 5; Figure 1).
It is reasonable to generalize from our results to other population
groups. We excluded underweight participants in an effort to provide a healthy
comparison group of normal weight, but the Framingham population sample is
largely a middle-class, middle-aged white cohort. Different results might
be obtained in population samples with a different ethnic identity and in
the present era when hypertension, diabetes mellitus, and hypercholesterolemia
may be more effectively identified and treated. On the other hand, our data
may more accurately reflect the influence of adiposity on risk factors and
CVD not modified by treatment.
In summary, overweight and obesity were associated with an increased
RR for the development of cardiovascular risk factors and CVD itself. The
effects were consistently seen across cardiovascular end points and significant
adverse sequelae were typically observed even in persons who were overweight
but not obese, highlighting the importance for primary prevention and treatment
of moderate degrees of excess adiposity.
AUTHOR INFORMATION
Accepted for publication January 17, 2002.
From the National Heart, Lung, and Blood Institute's Framingham Heart
Study, supported by contract N01-HC-38038 from the National Institutes of
Health National Heart, Lung, and Blood Institute; grant AR/AG 41398 from the
National Institutes of Health; and a grant from Roche Laboratories, Nutley,
NJ.
Corresponding author: Peter W. F. Wilson, MD, Boston University School
of Medicine, 715 Albany St, Evans 204, Boston, MA 02118 (e-mail: pwilson{at}bumc.bu.edu).
From the Boston University School of Medicine (Drs Wilson and Kannel),
and the Department of Mathematics, Boston University (Drs D'Agostino, Sullivan,
and Parise), Boston, Mass.
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Energy Metabolism in Human Renin-Gene Transgenic Rats: Does Renin Contribute to Obesity?
Gratze et al.
Hypertension 2009;53:516-523.
ABSTRACT
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Dissociation Between Sympathetic Nerve Traffic and Sympathetically Mediated Vascular Tone in Normotensive Human Obesity
Agapitov et al.
Hypertension 2008;52:687-695.
ABSTRACT
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Insulin Therapy, Hyperglycemia, and Hypertension in Type 1 Diabetes Mellitus
de Boer et al.
Arch Intern Med 2008;168:1867-1873.
ABSTRACT
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The Relationship Between Obesity and Atherosclerotic Progression and Prognosis Among Patients With Coronary Artery Bypass Grafts: The Effect of Aggressive Statin Therapy
Wee et al.
J Am Coll Cardiol 2008;52:620-625.
ABSTRACT
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Overweight, Obesity, and the Risk of Recurrent Venous Thromboembolism
Eichinger et al.
Arch Intern Med 2008;168:1678-1683.
ABSTRACT
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Age-Related Differences in Arterial Compliance Are Independent of Body Mass Index
Fjeldstad et al.
ANGIOLOGY 2008;59:454-458.
ABSTRACT
Prediction of First Events of Coronary Heart Disease and Stroke With Consideration of Adiposity
Wilson et al.
Circulation 2008;118:124-130.
ABSTRACT
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Body Mass Index, Abdominal Adiposity, Obesity, and Cardiovascular Reactions to Psychological Stress in a Large Community Sample
Carroll et al.
Psychosom. Med. 2008;70:653-660.
ABSTRACT
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Obesity, Behavioral Lifestyle Factors, and Risk of Acute Coronary Events
Jensen et al.
Circulation 2008;117:3062-3069.
ABSTRACT
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The Joint Effects of Physical Activity and Body Mass Index on Coronary Heart Disease Risk in Women
Weinstein et al.
Arch Intern Med 2008;168:884-890.
ABSTRACT
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Underweight, overweight and obesity as risk factors for mortality and hospitalization
Ringback Weitoft et al.
Scand J Public Health 2008;36:169-176.
ABSTRACT
Visceral Adipose Tissue Inflammation Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice
Ohman et al.
Circulation 2008;117:798-805.
ABSTRACT
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Is the obesity epidemic exaggerated? No
Jeffery and Sherwood
BMJ 2008;336:245-245.
FULL TEXT
Guidelines improve general trend of lowered cholesterol levels in type 2 diabetes patients in spite of low adherence
Fharm et al.
Scand J Public Health 2008;36:69-75.
ABSTRACT
State of the Art Reviews: Relationship Between Diet/ Physical Activity and Health
O'Neil and Nicklas
AMERICAN JOURNAL OF LIFESTYLE MEDICINE 2007;1:457-481.
ABSTRACT
Diabetes, the Metabolic Syndrome, and Ischemic Stroke: Epidemiology and possible mechanisms
Air and Kissela
Diabetes Care 2007;30:3131-3140.
FULL TEXT
Cause-Specific Excess Deaths Associated With Underweight, Overweight, and Obesity
Flegal et al.
JAMA 2007;298:2028-2037.
ABSTRACT
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Keeping the young-elderly healthy: is it too late to improve our health through nutrition?
Rivlin
Am. J. Clin. Nutr. 2007;86:1572S-1576S.
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Forgotten but Not Gone: The Rediscovery of Fatty Heart, the Most Common Unrecognized Disease in America
Szczepaniak et al.
Circ. Res. 2007;101:759-767.
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State of the Art Review: Long-term Pharmacotherapy for Overweight and Obesity: A Review of Sibutramine, Orlistat, and Rimonabant
Dunican et al.
AMERICAN JOURNAL OF LIFESTYLE MEDICINE 2007;1:367-388.
ABSTRACT
Urban--rural differences in BMI, overweight and obesity in Norway (1990 and 2001)
Svensson et al.
Scand J Public Health 2007;35:555-558.
ABSTRACT
Visceral and Subcutaneous Adipose Tissue Volumes Are Cross-Sectionally Related to Markers of Inflammation and Oxidative Stress: The Framingham Heart Study
Pou et al.
Circulation 2007;116:1234-1241.
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Cardiac Energy Metabolism in Obesity
Lopaschuk et al.
Circ. Res. 2007;101:335-347.
ABSTRACT
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Less weight or more hype with {blacktriangledown}rimonabant?
DTB 2007;45:41-44.
ABSTRACT
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Obesity, Inflammation, and Periodontal Disease
Pischon et al.
JDR 2007;86:400-409.
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Association of Ethnicity and Socioeconomic Status with Judgments of Body Size: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Lynch et al.
Am J Epidemiol 2007;165:1055-1062.
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Changes in Body Composition in Women over Six Years at Midlife: Ovarian and Chronological Aging
Sowers et al.
J. Clin. Endocrinol. Metab. 2007;92:895-901.
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Adiponectin and risk of acute coronary syndromes: defining the obesity phenotype
Pischon and Rimm
Eur Heart J 2007;28:274-275.
FULL TEXT
What Predicts Progression and Regression of Urinary Albumin Excretion in the Nondiabetic Population?
Brantsma et al.
J. Am. Soc. Nephrol. 2007;18:637-645.
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The Inhibitory Effect of Leptin on Angiotensin II-Induced Vasoconstriction in Vascular Smooth Muscle Cells Is Mediated via a Nitric Oxide-Dependent Mechanism
Rodriguez et al.
Endocrinology 2007;148:324-331.
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Left Ventricular Hypertrophy in Severe Obesity: Interactions Among Blood Pressure, Nocturnal Hypoxemia, and Body Mass
Avelar et al.
Hypertension 2007;49:34-39.
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Weight-change as a prognostic marker in 12 550 patients following acute myocardial infarction or with stable coronary artery disease
Kennedy et al.
Eur Heart J 2006;27:2755-2762.
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A Proinflammatory State Is Detectable in Obese Children and Is Accompanied by Functional and Morphological Vascular Changes
Kapiotis et al.
Arterioscler. Thromb. Vasc. Bio. 2006;26:2541-2546.
ABSTRACT
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Obesity and Sepsis
Vachharajani and Vital
J Intensive Care Med 2006;21:287-295.
ABSTRACT
The medical complications of obesity
Malnick and Knobler
QJM 2006;99:565-579.
FULL TEXT
Cardiorespiratory Fitness and Short-term Complications After Bariatric Surgery.
McCullough et al.
Chest 2006;130:517-525.
ABSTRACT
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Cockroft-Gault or abbreviated-MDRD equations--which 'weighs' more in cardiovascular risk?
Rodrigo and Andres
Nephrol Dial Transplant 2006;21:2342-2343.
FULL TEXT
Medical Risks in Living Kidney Donors: Absence of Proof Is Not Proof of Absence
Ommen et al.
CJASN 2006;1:885-895.
ABSTRACT
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Combining Risk Estimates from Observational Studies with Different Exposure Cutpoints: A Meta-analysis on Body Mass Index and Diabetes Type 2
Hartemink et al.
Am J Epidemiol 2006;163:1042-1052.
ABSTRACT
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Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss.
Poirier et al.
Arterioscler. Thromb. Vasc. Bio. 2006;26:968-976.
ABSTRACT
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Adiponectin: a promising marker for cardiovascular disease.
Pischon and Rimm
Clin. Chem. 2006;52:797-799.
FULL TEXT
Adiposity of the Heart*, Revisited
McGavock et al.
ANN INTERN MED 2006;144:517-524.
ABSTRACT
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Metabolic Syndrome: Connecting and Reconciling Cardiovascular and Diabetes Worlds
Grundy
J Am Coll Cardiol 2006;47:1093-1100.
ABSTRACT
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Long-term Changes in Blood Pressure in Extremely Obese Patients Who Have Undergone Bariatric Surgery.
Fernstrom et al.
Arch Surg 2006;141:276-283.
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Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss: An Update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease From the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism
Poirier et al.
Circulation 2006;113:898-918.
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Commentary: Obesity and cardiovascular disease risk among the young and old--is BMI the wrong benchmark?
Flint and Rimm
Int J Epidemiol 2006;35:187-189.
FULL TEXT
Risk Factors for Arterial Hypertension in Adults With Initial Optimal Blood Pressure: The Strong Heart Study
de Simone et al.
Hypertension 2006;47:162-167.
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Are waist circumference and body mass index independently associated with cardiovascular disease risk in Chinese adults?
Wildman et al.
Am. J. Clin. Nutr. 2005;82:1195-1202.
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Disorders of glucose metabolism in sleep apnea
Punjabi and Polotsky
J. Appl. Physiol. 2005;99:1998-2007.
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Depressive Symptoms and 24-Hour Urinary Norepinephrine Excretion Levels in Patients With Coronary Disease: Findings From the Heart and Soul Study
Otte et al.
Am. J. Psychiatry 2005;162:2139-2145.
ABSTRACT
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Is there a pathophysiological role for perivascular adipocytes?
Engeli
Am. J. Physiol. Heart Circ. Physiol. 2005;289:H1794-H1795.
FULL TEXT
Relation of Characteristics of Metabolic Syndrome to Short-Term Prognosis and Effects of Intensive Statin Therapy After Acute Coronary Syndrome: An analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial
Schwartz et al.
Diabetes Care 2005;28:2508-2513.
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Activation of the Peripheral Endocannabinoid System in Human Obesity
Engeli et al.
Diabetes 2005;54:2838-2843.
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Which anthropometric measurements is most closely related to elevated blood pressure?
Yalcin et al.
Fam Pract 2005;22:541-547.
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Is Prehypertension a Risk Factor for Cardiovascular Diseases?
Qureshi et al.
Stroke 2005;36:1859-1863.
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Weight Management Using Lifestyle Modification in the Prevention and Management of Type 2 Diabetes: Rationale and Strategies
The American Diabetes Association et al.
Clin. Diabetes 2005;23:130-136.
FULL TEXT
Adipose Tissue Metabolism and CD11b Expression on Monocytes in Obese Hypertensives
Boschmann et al.
Hypertension 2005;46:130-136.
ABSTRACT
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Re: "(Mis)use of Factor Analysis in the Study of Insulin Resistance Syndrome"
Hanley et al.
Am J Epidemiol 2005;161:1182-1184.
FULL TEXT
Comparative Impact of Morbid Obesity vs Heart Failure on Cardiorespiratory Fitness
Gallagher et al.
Chest 2005;127:2197-2203.
ABSTRACT
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Is the Kidney Always the Cause of Hypertension?: Distinct Roles for the Kidney and Systemic Tissues in Blood Pressure Regulation by the Renin-Angiotensin System. J Clin Invest 115: 1092-1099, 2005
Crowley et al.
J. Am. Soc. Nephrol. 2005;16:1525-1532.
FULL TEXT
The Increasing Medical Burden in Bipolar Disorder
Kupfer
JAMA 2005;293:2528-2530.
FULL TEXT
Secular Trends in Cardiovascular Disease Risk Factors According to Body Mass Index in US Adults
Gregg et al.
JAMA 2005;293:1868-1874.
ABSTRACT
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Fatness Is a Better Predictor of Cardiovascular Disease Risk Factor Profile Than Aerobic Fitness in Healthy Men
Christou et al.
Circulation 2005;111:1904-1914.
ABSTRACT
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Body Build and Risk of Cardiovascular Events in Hypertension and Left Ventricular Hypertrophy: The LIFE (Losartan Intervention For Endpoint reduction in hypertension) Study
de Simone et al.
Circulation 2005;111:1924-1931.
ABSTRACT
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Weight Loss and the Renin-Angiotensin-Aldosterone System
Engeli et al.
Hypertension 2005;45:356-362.
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Overweight and obesity and weight change in middle aged men: impact on cardiovascular disease and diabetes
Wannamethee et al.
J. Epidemiol. Community Health 2005;59:134-139.
ABSTRACT
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Weight Change Is Associated With Change in Arterial Stiffness Among Healthy Young Adults
Wildman et al.
Hypertension 2005;45:187-192.
ABSTRACT
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The prognostic importance of body mass index after complicated myocardial infarction
Kennedy et al.
J Am Coll Cardiol 2005;45:156-158.
FULL TEXT
Joint effects of physical activity, body mass index, waist circumference and waist-to-hip ratio with the risk of cardiovascular disease among middle-aged Finnish men and women
Hu et al.
Eur Heart J 2004;25:2212-2219.
ABSTRACT
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Weight Loss Reduces Circulating Asymmetrical Dimethylarginine Concentrations in Morbidly Obese Women
Krzyzanowska et al.
J. Clin. Endocrinol. Metab. 2004;89:6277-6281.
ABSTRACT
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Relationship Between Obesity and B-Type Natriuretic Peptide Levels
McCord et al.
Arch Intern Med 2004;164:2247-2252.
ABSTRACT
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Appropriate body mass index and waist circumference cutoffs for categorization of overweight and central adiposity among Chinese adults
Wildman et al.
Am. J. Clin. Nutr. 2004;80:1129-1136.
ABSTRACT
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Activation of the systemic and adipose renin-angiotensin system in rats with diet-induced obesity and hypertension
Boustany et al.
Am. J. Physiol. Regul. Integr. Comp. Physiol. 2004;287:R943-R949.
ABSTRACT
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Thirty-year Trends in Cardiovascular Risk Factor Levels among US Adults with Diabetes: National Health and Nutrition Examination Surveys, 1971-2000
Imperatore et al.
Am J Epidemiol 2004;160:531-539.
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Weight management through lifestyle modification for the prevention and management of type 2 diabetes: rationale and strategies. A statement of the American Diabetes Association, the North American Association for the Study of Obesity, and the American Society for Clinical Nutrition
Klein et al.
Am. J. Clin. Nutr. 2004;80:257-263.
ABSTRACT
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Weight Management Through Lifestyle Modification for the Prevention and Management of Type 2 Diabetes: Rationale and Strategies: A statement of the American Diabetes Association, the North American Association for the Study of Obesity, and the American Society for Clinical Nutrition
Klein et al.
Diabetes Care 2004;27:2067-2073.
FULL TEXT
A Practical and Evidence-Based Approach to Cardiovascular Disease Risk Reduction
Gluckman et al.
Arch Intern Med 2004;164:1490-1500.
ABSTRACT
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Effectiveness Of A Disease Management Program For Patients With Diabetes
Villagra and Ahmed
Health Aff (Millwood) 2004;23:255-266.
ABSTRACT
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Obesity and Hypertension-Induced Restrictive Cardiomyopathy: A Harbinger of Things to Come
Pilz et al.
Hypertension 2004;43:911-917.
FULL TEXT
Association of weight change with ethnicity and life course socioeconomic position among Brazilian civil servants
Chor et al.
Int J Epidemiol 2004;33:100-106.
ABSTRACT
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Adiposity Contributes to Differences in Left Ventricular Structure and Diastolic Function with Age in Healthy Men
Gates et al.
J. Clin. Endocrinol. Metab. 2003;88:4884-4890.
ABSTRACT
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Measures of Obesity Are Associated With Vascular Stiffness in Young and Older Adults
Wildman et al.
Hypertension 2003;42:468-473.
ABSTRACT
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The Metabolic Syndrome: A Practical Guide to Origins and Treatment: Part II
Wilson and Grundy
Circulation 2003;108:1537-1540.
FULL TEXT
Obesity and the Metabolic Syndrome
Keller and Lemberg
Am J Crit Care 2003;12:167-170.
FULL TEXT
Intakes of Calcium and Vitamin D Predict Body Mass Index in the Population of Northern Norway
Kamycheva et al.
J. Nutr. 2003;133:102-106.
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