The Obesity Epidemic: Pathophysiology and
Consequences of Obesity
F. Xavier Pi-Sunyer
Abstract
PI-SUNYER, F. XAVIER. The obesity epidemic:
pathophysiology and consequences of obesity. Obes Res.
2002;10:97S–104S.
Obesity has reached epidemic proportions in the United
States: more than 20% of adults are clinically obese as
defined by a body mass index of 30 kg/m2 or higher, and an
additional 30% are overweight. Environmental, behavioral,
and genetic factors have been shown to contribute to the
development of obesity. Elevated body mass index, partic-
ularly caused by abdominal or upper-body obesity, has been
associated with a number of diseases and metabolic abnor-
malities, many of which have high morbidity and mortality.
These include hyperinsulinemia, insulin resistance, type 2
diabetes, hypertension, dyslipidemia, coronary heart dis-
ease, gallbladder disease, and certain malignancies. This
underscores the importance of identifying people at risk for
obesity and its related disease states.
Key words: obesity, abdominal obesity, body mass in-
dex, insulin resistance, epidemiology
Introduction
The obesity epidemic in the United States is an unin-
tended consequence of the economic, social, and technolog-
ical advances realized during the past several decades. The
food supply is low in cost and abundant, and palatable foods
with high caloric density are readily available in prepack-
aged forms and in fast-food restaurants. Labor-saving tech-
nologies have greatly reduced the amount of physical ac-
tivity that used to be part of everyday life. Finally, the
Division of Endocrinology, Diabetes, and Nutrition, New York Obesity Research Center,
Columbia University College of Physicians and Surgeons, St. Luke’s-Roosevelt Hospital
Center, New York, New York.
Address correspondence to F. Xavier Pi-Sunyer, MD, Division of Endocrinology, Diabetes
and Nutrition, New York Obesity Research Center, Columbia University College of Phy-
sicians and Surgeons, St. Luke’s-Roosevelt Hospital Center, 111 Amsterdam Avenue, 10th
Floor, New York, NY 10025.
E-mail: fxp1@columbia.edu
Copyright © 2002 NAASO
OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002
widespread availability of electronic devices in the home has
promoted a sedentary lifestyle, particularly among children.
The prevalence of obesity, which is defined as a body
mass index (BMI) of 30 kg/m2 or higher, has been increas-
ing dramatically. According to the Behavioral Risk Factor
Surveillance System, a cross-sectional telephone survey of
noninstitutionalized adults ages 18 years or older conducted
by the Centers for Disease Control and Prevention, the
prevalence of obesity between 1991 and 1998 increased in
all 50 states in the United States, in both men and women,
and across all age groups (1). Notably, only 4 states had
obesity rates of 15% or higher in 1991, but by 1998, 37
states had exceeded that level. The National Health and
Nutrition Examination Surveys (NHANES) show that the
prevalence of obesity rose gradually from 1960 to 1980, but
in the period from the second survey (NHANES II: 1976 to
1980) until the third (NHANES III: 1988 to 1994), it in-
creased markedly, from 14.5% to 22.5% (2). The increase in
obesity prevalence noted in the NHANES surveys was also
evident in both men and women, across all age groups, and
across race-ethnic groups (Figure 1). The highest prevalence
of obesity was found among women of minority groups.
The combined prevalence of overweight (BMI, 25 to 29.9
kg/m2) and obesity also increased dramatically, from 46.0%
to 54.4% in the period from the second to third NHANES
surveys (2). The rates of overweight and obesity were
highest among black women and Mexican-American men
and women.
BMI values in the United States population do not exhibit
a normal distribution; rather, there is an enormous burden of
higher BMI values that reflect the large percentage of peo-
ple who are overweight or obese. In NHANES III, the BMI
distribution included 16.0% with values of 25 to 27 kg/m2,
18.6% with values of 27 to 30 kg/m2, 16.1% with values of
30 to 34.9 kg/m2 (class I obesity), 5.1% with values of 35 to
39.9 kg/m2 (class II obesity), and 2.9% with values in
excess of 40 kg/m2 (class III obesity) (3). Importantly, BMI
values are strongly correlated with total-body fat content,
indicating that the degree of obesity can be calculated
simply from height and weight measurements (4).
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Obesity Epidemic, Pi-Sunyer

Figure 1: Increasing prevalence of obesity during the past several decades. Panel A shows the age-adjusted prevalence according to gender
and race, and panel B shows the prevalence according to age group. Data are from the National Health Examination Survey (NHES) and
the three National Health and Nutrition Examination Surveys (NHANES) (2).

Pathophysiology of Obesity provides further evidence of the importance of genetics (7).

The weight class of the adoptees in adulthood was classified
Genetics vs. Environment
as thin, median, overweight, or obese. Notably, the weight
The relative contributions of genetics and environment to
class was strongly related to the BMI of their biological
the etiology of obesity have been evaluated in many studies.
parents, but it was unrelated to the BMI of their adoptive
Although it varies from study to study, ⬃30% to 40% of the
parents. In contrast, the weight of infants in their first 2
variance in BMI can be attributed to genetics and 60% to
years was unrelated to maternal or paternal BMI (8).
70% to environment. The interaction between genetics and
The impact of environment is illustrated by a study of
environment is also important. In a given population, some
Pima Indians (9); those residing in Arizona have among the
people are genetically predisposed to develop obesity, but
highest prevalence of obesity. Despite the similar genetic
that genotype may be expressed only under certain adverse
predisposition, Pima Indians living a traditional lifestyle in
environmental conditions, such as high-fat diets and seden-
tary lifestyles (5) (Figure 2). In the United States, as well as
in other Western countries, greater numbers of people are
being exposed to these adverse environmental conditions,
and consequently, the percentage of people expressing the
obesity genotype has increased.
The role of genetics is illustrated by a study of identical
young-adult male twins who were overfed by 1000 kcal/d
over a 100-day period (6). The weight gain among partici-
pants ranged from 4.3 to 13.3 kg, but the variance in
response was significantly lower within pairs of twins than
among pairs. The similarity in response within pairs was
evident for body weight, percentage of fat, fat mass, and
estimated subcutaneous fat. In other words, some twin pairs
gained much more weight than other pairs. The concordance
in response between identical twins demonstrates the impact Figure 2: The interaction of genetics and environment (5).
of genetics on weight gain. A study of 540 adult adoptees

98S OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002

Obesity Epidemic, Pi-Sunyer
a remote section of Mexico had significantly lower BMI
than those living in the more affluent environment of Ari-
zona (24.9 vs. 33.4 kg/m2; p ⬍ 0.001). These groups were
separated ⬃700 to 1000 years ago and now differ in terms
of both diet and energy expenditure. Pima Indians living in
Mexico eat a diet with less animal fat and caloric density
and more complex carbohydrates than those in Arizona,
and they also have greater energy expenditure from
physical labor.
Metabolic Predictors of Weight Gain
The development of obesity occurs when the caloric
intake is disproportionate to the energy expended. Three
metabolic factors have been reported to be predictive of
weight gain: a low adjusted sedentary energy expenditure, a
high respiratory quotient (RQ; carbohydrate-to-fat oxidation
ratio), and a low level of spontaneous physical activity.
The resting metabolic rate (RMR) is strongly correlated
to fat-free mass (FFM) in both men and women (10).
However, RMR is only one component of the total daily
energy expenditure, which also includes the thermic effect
of food and physical activity (11). Daily energy expenditure
can be measured in a respiratory chamber or in free-living
people by the doubly labeled water method. The contribu-
tion of low energy expenditure to the development of obe-
sity was evaluated in several studies of Pima Indians. In a
study of 95 subjects, the mean 24-hour adjusted energy
expenditure was 36.3 kcal/kg FFM, but it varied consider-
ably among the participants, from 28 to 42 kcal/kg FFM
(12). Notably, this thermogenic response was correlated
inversely with the change in body weight over a 2-year
follow-up (r ⫽ ⫺0.39, p ⬍ 0.001). People with low ad-
justed energy expenditure were four times more likely to
gain 7.5 kg during follow-up than those with high adjusted
energy expenditure. Similar results were found in a second
group of 126 subjects who were followed up for 4 years
(12). Of those with low RMR, 28% had a 10-kg body
weight gain during follow-up compared with ⬍5% of those
with high RMR. Finally, in a group of 94 siblings from 36
families, the 24-hour energy expenditure tended to aggre-
gate in families, such that some families showed low levels
and others had high levels of energy expenditure (12). This
finding suggests that energy expenditure may have a famil-
ial determinant.
The Pima Indians provide the most convincing evidence
relating low RMR to weight gain, but other studies have
failed to show the same relationship. For example, RMR
was evaluated in 24 overweight postmenopausal women
before and after reduction to a normal-weight state (13). The
RMR declined during energy restriction and weight loss,
but it returned to baseline once energy balance was restored
in the weight-reduced state. At this time, the RMRs among
women who lost weight were not significantly different
from the RMRs in a control group of never-overweight
OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002
women. After a mean follow-up of 4 years, the weight-
reduced women regained an average of 87% of their lost
weight, but the weight gain was unrelated to their RMRs.
Moreover, women in the control group had minimal weight
gain over the same period, although their RMRs were com-
parable. The studies in Pima Indians measured 24-hour
energy expenditure in a respiratory chamber. However,
when total energy expenditure under free-living conditions
was measured using the doubly labeled water method, total
energy expenditure/RMR ratios ⬎1.75 were associated with
lower BMI in men and less weight gain in previously obese
women (14).
RQ is the second potential metabolic predictor of weight
gain. A low RQ of 0.7 suggests that a person is oxidizing
more fat than carbohydrate, whereas a ratio of 1.0 suggests
that more carbohydrate than fat is being oxidized (11). The
relationship between RQ and weight gain was evaluated in
nondiabetic Pima Indians who were fed a weight-mainte-
nance diet (15). In a group of 152 subjects, the 24-hour RQ
varied from 0.799 to 0.903. Notably, the 24-hour RQ cor-
related with changes in body weight during a mean fol-
low-up of 25 months (r ⫽ 0.27, p ⬍ 0.01). Subjects in the
90th percentile of RQ were 2.5 times more likely to gain at
least 5 kg than those in the 10th percentile, and this effect
was independent of 24-hour energy expenditure.
It is believed that a sedentary lifestyle also has an impact on
weight gain, but it remains to be shown in a well-designed
longitudinal study. According to the 1996 Surgeon General’s
Report on Physical Activity and Health, participation in phys-
ical activity decreases with age. In each age group, more
women than men do not participate in physical activity. For
example, by the age of 45, ⬃18% of men and 30% of women
are not regularly engaged in physical activity.
Several other factors also are associated with overweight,
but it is not clear why or how they have an impact. Sex, age,
race, and socioeconomic status have an impact on weight
gain, with overweight and obesity being more likely among
women, older individuals, members of minority races, and
those of low socioeconomic status. In the Behavioral Risk
Factor Surveillance System, for example, the prevalence of
obesity in 1998 was 18.1% among women and 17.7%
among men (1). It increased from 12.1% among young
adults ages 18 to 29 years and reached a maximum of 23.8%
among those ages 50 to 59 years. African Americans had
higher rates of obesity than Hispanics, who in turn had
higher rates than whites. Finally, obesity prevalence de-
clined with increasing levels of education, ranging from
24.1% among those who did not complete high school to
13.1% among those who graduated from college.
Patterns of Body-Fat Distribution and Risk
for Certain Diseases
Obesity increases risk for many disorders that are asso-
ciated with high mortality and morbidity, including diabe-
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Obesity Epidemic, Pi-Sunyer
Table 1. Disorders associated with obesity [adapted
from Must et al. 1999; Pi-Sunyer 1993; USDHHS
2001 (16 –18)]
● Insulin ● Osteoarthritis
resistance/hyperinsulinemia ● Stroke
● Type 2 diabetes ● Asthma
● Hypertension ● Sleep apnea
● Dyslipidemia ● Breathing difficulties
● Coronary heart disease ● Complications of
● Gallbladder disease pregnancy
● Cancer (prostate, ● Menstrual
endometrial, uterine, irregularities
cervical, ovarian, colon, ● Hirsutism
kidney, gallbladder, and ● Increases surgical
postmenopausal breast) risk
● Premature death ● Psychological distress
tes, hypertension, coronary heart disease (CHD), dyslip-
idemia, gallbladder disease, and certain malignancies
(16 –18) (Table 1). Not only does excess weight increase
the risk of these disorders, but the pattern of fat distri-
bution is important in many of these conditions. Men are
more likely to have abdominal or upper-body obesity,
whereas women are more likely to have a gluteofemoral
or lower-body pattern of fat distribution. However, as
women gain weight, they become more likely to develop
abdominal and upper-body fat. There are now numerous
prospective longitudinal studies showing that a pattern of
upper-body fat distribution is independently associated
with higher risk of developing diabetes and cardiovascu-
lar disease (19 –24). Moreover, cross-sectional studies
show that abdominal fat distribution is related to various
metabolic abnormalities and disorders in a manner sim-
ilar to their relationship with high BMI or total fat burden
(25–27). These metabolic abnormalities include athero-
genic profile, high fibrinogen levels, hypertension, insu-
lin resistance, hyperinsulinemia, glucose intolerance, ar-
thritis, menstrual irregularities, and gallbladder disease.
Disorders Associated with Obesity
Insulin Resistance and Hyperinsulinemia
A reduction in sensitivity to insulin can occur through an
inherited defect, or it can be acquired as a consequence of
obesity. The impact of obesity is independent of genetic
factors, as illustrated by a study of 23 sets of identical twins
who were discordant for weight (28). Within both male and
female twin pairs, the obese member had higher fasting
insulin levels and showed lower insulin sensitivity in the
75-g oral glucose tolerance test than the non-obese member.
100S OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002
These differences were particularly evident among mem-
bers with high abdominal fat distribution. Once hyperinsu-
linemia and insulin resistance is acquired, it starts a cascade
of metabolic changes that leads to diabetes, dyslipidemia,
hypertension, hypercoagulability, and eventually cardiovas-
cular disease.
The relationship between insulin sensitivity and BMI
is illustrated using the minimal model technique of
Bergman (29). In a group of nondiabetic persons whose
BMI ranged widely, insulin sensitivity was inversely
correlated with BMI (30). The lower insulin sensitivity
in obese subjects is also evident when insulin levels are mea-
sured over a 24-hour period (31). In both the fasting and
postprandial states, obese subjects require insulin levels that
are several times higher than non-obese subjects to maintain
normal glucose tolerance.
On a cellular level, insulin binds to its receptor on the
surface of target cells, thereby causing tyrosine autophos-
phorylation and consequent intracellular signaling. These
events culminate in cellular responses, such as the trans-
location of glucose transporters to the cell surface to
allow glucose uptake for use or glycogen storage. In
obesity, however, insulin signaling is defective. Insulin-
stimulated protein kinase activity of the insulin receptor,
which mediates tyrosine autophosphorylation, is reduced
in obese subjects relative to non-obese ones, and it is
further reduced in obese type 2 diabetes patients (32).
Furthermore, obesity is associated with other postrecep-
tor binding defects in insulin action, including impaired
generation of second messengers, diminished glucose
transport, and abnormalities in some critical enzymatic
steps involved in glucose use (33,34). Abnormalities in
lipogenesis and protein synthesis also occur in obesity
(35). However, obese subjects with depressed insulin-
mediated glucose transport can recover this response
after weight loss (33).
The increased levels of free fatty acids (FFAs) found in
obese individuals also contribute to the defects in glucose
use and storage. As body fat increases, the rate of lipolysis
rises, leading to increased FFA mobilization and conse-
quently to increased FFA oxidation in muscle and liver
(Figure 3). In turn, glucose use by muscle declines as FFA
is used as an alternate energy source, and hepatic glucose
production increases in response to the higher FFA oxida-
tion. These actions result in hyperglycemia and impaired
glucose tolerance. This mechanism is particularly important
among individuals with upper-body obesity. The plasma
FFA turnover rate was higher among women with upper-
body obesity compared with those with lower-body obesity
or non-obese women (36). Moreover, the women with up-
per-body obesity showed lower glucose disposal and greater
hepatic glucose production than the women with lower-
body obesity, who in turn had smaller defects than the
Obesity Epidemic, Pi-Sunyer
Figure 3: Effect of increased lipolysis on glucose use and gluconeogenesis.
non-obese controls (36,37). Thus, obesity—particularly ab-
dominal or upper-body obesity—increases risk for glucose
intolerance.
Type 2 Diabetes
The relative risk of developing type 2 diabetes increases
steeply with increasing BMI. This relationship is best dem-
onstrated by the Nurses’ Health Study, which prospectively
followed up more than 114,000 registered nurses for 14
years (38). Relative to women with BMI ⬍22 kg/m2, age-
adjusted risk of developing type 2 diabetes rose steadily
with increasing BMI. Women with BMI of 35 kg/m2 or
greater had a 93 times higher risk of developing diabetes
than those with BMI of ⬍22 kg/m2. Even women who were
overweight had higher risk; those with BMI of 25.0 to 26.9
kg/m2 and 27.0 to 28.9 kg/m2 had relative risks of 8.1 and
15.8, respectively. Weight gain is also important in deter-
mining risk of diabetes, particularly among those with
higher baseline BMI. In a study of more than 51,000 male
health professionals ages 40 to 75 years, subjects were
grouped into tertiles according to their BMI at age 21 (39).
Diabetes risk was positively correlated with absolute weight
gain since age 21 in each tertile as well as with BMI at age
21. Subjects with a BMI of 24 kg/m2 or higher at age 21
who gained at least 11 kg had a 21 times higher risk of
developing diabetes than those with a BMI of ⬍22 kg/m2
who gained ⬍5 kg since age 21.
Abdominal obesity, as measured by waist-to-hip ratio,
may be a stronger predictor of diabetes than BMI alone. In
the Study of Men Born in 1913, a cohort of 54-year-old men
were followed for 13.5 years (20); subjects were grouped
OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002
into tertiles of baseline BMI and waist-to-hip ratio. Subjects
in the lowest tertile of waist-to-hip ratio did not have in-
creased risk of developing diabetes, even if they were in the
highest BMI tertile. However, in each of the other tertiles of
waist-to-hip ratio, increasing BMI was associated with a
greater probability of developing diabetes. Notably, the
relative risk of developing diabetes was 30 times higher
among those with the highest BMI and waist-to-hip ratio
compared with those with the lowest waist-to-hip ratio.
Hypertension
The risk of hypertension also increases with increasing
BMI. In the Nurses’ Health Study, risk of developing hy-
pertension was determined among 41,541 predominantly
white female nurses ages 38 to 63 years (40). During a
4-year follow-up, the risk of hypertension was increased
among overweight and obese women relative to those with
a BMI of ⬍23 kg/m2. The relative risk was 4.8 for those
with BMI of 32 kg/m2 or higher. In addition to BMI, weight
gain also dramatically increased risk of hypertension in each
tertile of initial BMI, and weight loss reduced such risk (41).
The NHANES III data also show that obesity increases risk
of hypertension (42). Respondents with BMI of 30 kg/m2 or
greater were twice as likely to have hypertension compared
with non-obese subjects. Similarly, subjects with abdominal
obesity, defined by a waist circumference of at least 102 cm
for men and 88 cm for women, were twice as likely to have
hypertension. The relationship among BMI, abdominal obe-
sity, and the odds ratio for hypertension was evident among
whites, African Americans, and Hispanics.
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Obesity Epidemic, Pi-Sunyer
The hypertension associated with obesity is characterized
by an increase in vascular volume, whereas peripheral re-
sistance is generally borderline or only slightly elevated
(41). Several mechanisms may be involved in the develop-
ment of hypertension in obese subjects: increased renal
sodium and water absorption, sympathetic nervous system
activation, changes in Na⫹/H⫹-ATPase activity, and growth
factor–mediated structural changes to the vascular wall. In
each case, hyperinsulinemia may be a contributing factor.
Dyslipidemia
Impaired glucose use and increased hepatic glucose out-
put are not the only consequences of the higher FFA levels
in obesity. Increased FFAs also affect lipid metabolism by
increasing very-low-density lipoprotein production by the
liver, reducing high density lipoprotein (HDL)-cholesterol
levels, and increasing the number of small, dense low-
density lipoprotein (LDL) particles (43). These smaller par-
ticles are better able to penetrate the arterial wall, more
readily undergo oxidation and glycation, and are more
atherogenic than larger, buoyant LDL particles. Even when
the LDL cholesterol level does not change appreciably, athero-
genic risk may be higher because of the presence of the smaller
LDL particles. Taken together, these changes in lipoprotein
profile are associated with increased risk of CHD.
The impact of obesity on lipid metabolism is illustrated
by a study of women with low or high abdominal obesity
(44). The abdominal fat area in these two groups was 107
and 187 cm2, respectively. A control group of non-obese
women had an abdominal fat area of 50 cm2. The women
with high abdominal obesity had higher triglycerides and
lower HDL-cholesterol levels than those with low abdom-
inal obesity, which were in turn abnormal relative to the
non-obese group. LDL-cholesterol was increased modestly
in the obese women, but the LDL particles were more dense
and atherogenic.
CHD
Fasting insulin levels are related directly to CHD mortal-
ity. In the Paris Prospective Study, for example, which
evaluated CHD risk factors in more than 7000 working men,
fasting insulin levels were an independent predictor of CHD
death (45). Among those in the highest quintile of fasting
insulin (⬎19 ␮U/mL), the incidence of CHD mortality was
2.5 times higher than among men with insulin of 5 ␮U/mL
or less. Similarly, the fasting insulin level was found to be
an independent risk factor for developing CHD in a case-
control study of Canadian men (46). Even after adjusting for
plasma triglycerides, apolipoprotein B, LDL-cholesterol,
and HDL-cholesterol, the insulin level remained indepen-
dently associated with CHD risk.
A relationship between obesity and CHD mortality was
demonstrated in the Nurses’ Health Study among women
who had never smoked (47). The relative risk of CHD death
102S OBESITY RESEARCH Vol. 10 Suppl. 2 December 2002
increased significantly with increasing BMI (p ⬍ 0.001).
Women with BMI of 29.0 to 31.9 kg/m2 and 32.0 kg/m2 or
higher were at 4.6 and 5.8 times greater risk, respectively,
than those with BMI values under 22.0 kg/m2. Moreover,
the waist-to-hip ratio was strongly predictive of CHD mor-
tality. Women in the highest quintile of waist-to-hip ratio
had a relative risk of CHD death of 8.7 compared with those
in the lowest quintile.
Gallbladder Disease
An independent relationship between obesity and gall-
bladder disease was shown recently in the Atherosclerosis
Risk in Communities Study, which involved more than
12,700 subjects ages 45 to 64 years (48). In women, the risk
of hospitalization for gallbladder disease increased with
increasing BMI as well as higher waist-to-hip ratio. Over-
weight women had a 45% greater risk of hospitalization for
gallbladder disease than those with BMI ⬍ 25 kg/m2.
Among obese women, the risk increased further in relation
to BMI; those who were morbidly obese had a relative risk
of 2.5. Women with waist-to-hip ratios in the upper two
quartiles had a 2-fold higher risk than those in the lowest
quartile. In men, the relationship between BMI and risk of
hospitalization for gallbladder disease was only seen among
the morbidly obese group. The waist-to-hip ratio did not
influence risk among men.
Cancer
The impact of obesity on cancer mortality was evaluated
prospectively in a study of 750,000 men and women who
were followed for 12 years (49). Men and women who were
at least 40% overweight were 33% and 55% more likely,
respectively, to die from cancer than those of average
weight. Specifically, the mortality ratios for colorectal and
prostate cancer in men and endometrial, uterine, cervical,
ovarian, gallbladder, and breast cancer in women were
highest among those who were at least 40% overweight.
The highest mortality ratios were found for endometrial and
uterine cancer. Similarly, in the Nurses’ Health Study, can-
cer mortality increased with increasing BMI (47). The can-
cer death rate for women with BMI of at least 32 kg/m2 was
twice that for women with BMI of less than 19 kg/m2. The
higher rate was predominantly because of increased mortal-
ity caused by colon, breast, and endometrial cancers.
All-Cause Mortality
In a study of 750,000 men and women, mortality due to
any cause increased with higher body weight (50). In the
Nurses’ Health Study, all-cause mortality showed a
J-shaped relationship between BMI and overall mortality
(47). The lowest mortality was found among women with
BMI of 19.0 to 26.9 kg/m2, but then mortality increased
steadily as BMI levels rose above 27 kg/m2.
Obesity Epidemic, Pi-Sunyer
Summary
Several epidemiological surveys show that the prevalence
of overweight and obesity has been increasing over the past
two decades. The causes are multifactorial, but environmen-
tal, behavioral, and genetic factors have all been shown to
contribute. Several risk factors for obesity are known, in-
cluding a sedentary lifestyle, increasing age, and low socio-
economic status. These can help physicians identify which
patients are obese or at risk of developing obesity. Elevated
BMI and abdominal obesity are associated with a number of
diseases and metabolic abnormalities that have high mor-
bidity and mortality. This fact alone underscores the impor-
tance of the battle against the obesity epidemic.
Acknowledgments
Supported by NIH grants DK26687 and DK40414.
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