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Chapter 33. Epidemiology of Obesity
CHAPTER OUTLINE
Introduction
The global epidemic of obesity is one of the most significant public health threats of the
21st century. Fueled primarily by excess calories and physical inactivity, the dramatic increase in
overweight and obesity of the past several decades is considered the major cause for the parallel
rise in incident and prevalent diabetes Obesity, which is a strong, independent, and modifiable
predictor of type 2 diabetes, is also associated with numerous other serious chronic diseases and
health conditions such as cardiovascular diseases, some cancers, musculoskeletal,
gastrointestinal, respiratory, dermatologic, and reproductive disorders, social stigma, and
psychological distress.
Even more disturbing than increasing obesity in adults is the alarming rise in the
prevalence of childhood and adolescent overweight and obesity. Increasing obesity levels in
children have contributed to a much earlier onset of obesity-related diseases, diseases that were
previously diagnosed only in older adults.
Classification of Overweight and Obesity in Adults
The World Health Organization defines obesity as excessive body fat which has
accumulated to the point where health is negatively affected. The body mass index (BMI), which
is a ratio of the weight in kilograms to the square of the height in meters, BMI=kg/(m2), is the
global metric used for measuring and classifying levels of adiposity and associated obesityrelated chronic disease risk among adults. Obesity in children is measured differently using
percentile cut points based upon standardized growth charts for boys and girls.
Limitations of the Body Mass Index (BMI)
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Although the BMI is currently the universally accepted obesity metric, , it is not without
ribed limitations since it does not really measure body fat. Thus, people with increased muscle
mass, such as bodybuilders, are likely to be misclassified as overweight or obese, whereas fat
mass could be underestimated for those who have lost lean mass due to infirmity, sedentary
lifestyle, or increasing age.
The adult BMI cut points for being overweight (BMI of 25-30) or obese (BMI>30) are
derived primarily from studies of Caucasians, but these may be inaccurate for other ethnic
groups. For example, comparative studies have consistently shown that, on average, Asians have
higher percentages of body fat than Caucasians at corresponding levels of BMI.
Global Burden of Adult Obesity
The most recent global data reflect persisting upward trends in the numbers of
overweight and obese adults and clearly indicate that the worldwide obesity pandemic is
continuing unabated in the 21st century. In 2000, there were approximately 750 million
overweight and 300 million obese adults, ages 15 years or older whereas five years later in 2005,
1 billion adults were overweight and more than 400 million were obese. Thus, obesity is
increasing at an annual rate of about 6.6%.
Global Prevalence of Adult Obesity
In 2005, 937 million adults (23.2%) were overweight and 396 million (9.8%) were obese
in the world population. The prevalence of obesity was higher in women (11.2%) than men
(7.7%).
The development of obesity is related to an imbalance between calories consumed versus
calories expended or energy input versus energy output. Notably, the per capita dietary energy
supply has increased significantly in nearly all parts of the world during the past five decades,
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closely paralleling emergence of the global obesity epidemic.
Gender Differences in Obesity
The prevalence of obesity in women exceeds that in men by 5-10% at all ages. The
gender difference in obesity is widely recognized and has been attributed to evolutionary
pressures that predispose women to store excess fat for reproduction and lactation. Recent
studies suggest that gender differences in the distribution of body fat are largely determined by
differences in sex hormones. In postmenopausal women, abdominal/visceral adiposity increases
with the loss of ovarian estrogens whereas in men, the gradual decline in circulating androgens
with aging predisposes to the accumulation of abdominal fat.
Urban versus Rural Differences in Obesity
Based upon population studies within nations, the prevalence of obesity is much higher in
urban areas than in rural areas, even in low prevalence countries.
Prevalence of Adult Obesity in the United States
In the United States, the prevalence of obesity has more than doubled since 1960, when
only 13.3% of the adult population was classified as obese. In sharp contrast, the prevalence of
obesity in 2008 exceeded 30% in most states for men and women of most age groups.
Distribution of Obesity by Age, Gender and Ethnicity in the United States
The prevalence of obesity is disproportionately higher in certain US age-gender-ethnic
groups than others. The prevalence is particularly high (about 60%) in African American women
age 60 and older; roughly double the levels in Caucasian and Hispanic women. In men and
women of all ages, African Americans have higher levels (44%) than Hispanics (39%) and
Caucasians (33%).
Compared to other gender-ethnic groups, the lifestyles of certain African American
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women appear to predispose them to excessive weight gain and the development of obesity. The
web of causation includes high intake of carbohydrates, sugar and fat in the diet, physical
inactivity, high stress, high parity, low vitamin D, lactose intolerance, depression, and perception
of body weight.
Health Consequences of Obesity
Obesity exerts deleterious effects on nearly every organ system of the body and is
associated with numerous health conditions including type 2 diabetes, cardiovascular diseases
(such as coronary heart disease, myocardial infarction, and stroke), gastroesophageal reflux
disease (GERD), obstructive sleep apnea, asthma, gall bladder and fatty liver disease, depression,
urinary incontinence, gout, polycystic ovarian syndrome, and osteoarthritis.
Obesity and Total Mortality
Obesity is strongly associated with increased morbidity, mortality, disability and
impaired quality of life. Recent cause-specific mortality data reported by the World Health
Organization suggest that overweight and obesity are responsible for 2.8 million deaths annually,
ranking fifth among the top ten leading causes of death worldwide. According to these estimates,
44% of the disease burden from diabetes, 23% of the disease burden from ischemic heart disease
and 7% to 41% of the disease burdens from many forms of cancer are attributable to overweight
and obesity.
People who are obese are at greater risk for developing major chronic life-threatening
diseases such as type 2 diabetes, cardiovascular diseases, and some cancers. Obesity most likely
leads to the onset of most, if not all chronic diseases through direct effects on metabolic
dysregulation expressed clinically as hypertension, insulin resistance, hyperinsulinemia,
hyperglycemia, dyslipidemia, and low grade chronic inflammation.
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Obesity and Type 2 Diabetes
Obesity is considered the strongest modifiable predictor of type 2 diabetes. Recent
estimates suggest that nearly 70% of cases in the United States are attributable to overweight and
obesity.
Obesity and Cardiovascular Disease
Obesity is a major risk factor for the development of cardiovascular diseases. Results of a
recent meta-analysis found that, compared to normal weight subjects, those who were obese
(BMI > 30) were 81% more likely to develop coronary heart disease.
The INTERHEART Study examined obesity and myocardial infarction among 12,461
cases and 13,637 controls ascertained from 52 countries and representing several major ethnic
groups. The effects of two measures of obesity were compared, BMI and waist-to-hip ratio. The
population attributable fraction estimated from the upper two quintiles of the waist-to-hip ratio
was 24.3% compared to only 7.7% for BMI. These results suggest that the waist-to-hip ratio is
superior to BMI as a predictor of myocardial infarction.
In a large prospective US study, 18% to 20% of the new cases of ischemic stroke were
attributable to excess adiposity, measured by BMI > 28.1, waist circumference > 100 cm, or
waist to hip ratio > 0.95.
Obesity and Cancer
According to a report from the American Institute of Cancer Research, more than
100,500 annual cases of cancer and 14 to 20% of all cancer deaths in the United States can be
attributed to excess body fat.
Obesity and Gastroesophageal Reflux Disease (GERD)
Abdominal adiposity is of particular importance in the pathogenesis of GERD and its
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progression. Magnanimous abdominal girth may cause hiatal hernia and excessive reflux of acid
from the stomach into the esophagus by increasing intra-abdominal pressure. Also, visceral fat is
more metabolically active than subcutaneous fat or peripheral fat, capable of producing a
multitude of bioactive proteins (adipokines), including pro-inflammatory cytokines.
Complications and co-morbid conditions of GERD include erosive esophagitis, Barrett’s
esophagus (progressive metaplasia and dysplasia of the lower esophagus) and esophageal
carcinoma.
Obesity and Obstructive Sleep Apnea
Obesity is a major risk factor for the development of obstructive sleep apnea. The
disorder is particularly prominent among men with abdominal obesity and has been shown to
improve or resolve with weight loss.
Obesity and Osteoarthritis
The strong association between obesity and osteoarthritis of the major weight-bearing
joints has been widely verified.
Obesity and Quality of Life
In addition to substantial morbidity and increased risk of premature mortality, obesity is
also associated with decreases in the overall quality of life.
Mechanisms of Pathogenesis in Obesity-Related Diseases
Obesity and excess weight increase the mechanical stress and strain on multiple systems
of the human body. For example, excess weight causes compression of blood vessels and body
organs thereby creating mechanical resistance and distortion of normal function.
Adipose tissue plays a critical role in whole body metabolic regulation and cellular
energy homeostasis. Adipose is an active endocrine organ that secretes a variety of pro-
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inflammatory bioactive proteins, collectively called adipokines or adipocytokines. Adipokines
such as leptin, resistin, adiponectin, interleukin-6 (IL-6) and tumor necrosis factor (TNF-a)
influence many physiologic processes including body weight homeostasis, insulin resistance,
lipid levels, blood pressure, coagulation, inflammation and atherosclerosis. Grossly enlarged
adipocytes associated with obesity release pro-inflammatory adipokines that simultaneously
promote atherogenesis and insulin resistance.
Obesity and Atherogenesis
In the human system, the presence of excess white adipose tissue (WAT) that is
characteristic of obesity has been found to induce a persistent state of low grade inflammation. In
obese individuals, elevated levels of circulating autocrine, paracrine and endocrine factors
derived primarily from the excess visceral WAT are capable of inducing sustained inflammation
and atherogenesis. The obesity-related pro-inflammatory milieu of WAT-derived cytokines and
adipokines (particularly IL-6) stimulates the production of C-reactive protein (CRP) by the liver.
C-reactive protein is an acute phase protein whose concentration in the blood is increased in
both acute and chronic inflammatory states. Inflammatory mediators derived from adipose and
linked to CRP play an important role in atherogenesis and the development of coronary heart
disease, and CRP has emerged as one of the most powerful predictors of cardiovascular risk.
Obesity and Insulin Resistance
As lipid-laden adipocytes reach their threshold of fat storage, the white adipose tissue
(WAT) releases a variety of pro-inflammatory adipokines and cytokines that contribute to insulin
resistance and the development of type 2 diabetes.
Overview of Adipocyte Regulatory Processes
White Adipose Tissue (WAT) is the repository or storage vesicle for excess energy in the
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form of triglycerides (triacylglycerol). Storage capacity of WAT depends upon both fat cell
number (cellularity) and fat cell size.
Fat Storage (Lipogenesis)
Excess fat is stored in the adipocytes (fat cells) of WAT by a process known as
lipogenesis. Insulin, produced by the beta (β)-cells of the pancreas, is secreted into the blood in
response to elevated blood glucose and is the prime mediator of adipocyte glucose uptake to
furnish the energy required for lipogenesis.
Fat Breakdown (Lipolysis)
When long-term energy intake does not meet energy requirements, stored triacylglycerol
within adipoctyes is broken down by hormone sensitive lipase to free fatty acids that are released
from the fat cell to be used for energy by tissues of the body. The overall process is called
lipolysis. Homeostatic regulation of lipogenesis and lipolysis depends upon the presence of
adequate normal functioning WAT. Elevated levels of circulating triglycerides and free fatty
acids may interfere with insulin-dependent glucose transport in muscle leading to insulin
resistance and type 2 diabetes.
Secretion of Adipokines by Adipoctyes
Adipocytes actively participate in maintaining energy homeostasis by synthesizing and
secreting a multitude of autocrine, paracrine, and endocrine signaling proteins such as hormones,
complement components, growth factors, and cytokines collectively called adipokines. Fat cells
secrete adipokines as a direct response to their energy storage capacity. As excess energy in the
form of triacylglycerol is stored in adipocytes, individual fat cells can increase tremendously in
size (undergo hypertrophy) with the ability to expand twenty-fold in diameter and over one
thousand-fold in volume. However, each cell can only store so much excess energy (as
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triacylglycerol) and when its storage capacity is surpassed, pro-inflammatory adipokines are
secreted.
The adipocyte response to hypertophy is an epigenetic phenomenon leading to the
overexpression of specific genes that encode pro-inflammatory adipokines. One factor that may
induce such genetic expression is the physical stress and strain that wounds the plasma
membrane of fat-laden cells. Indeed, plasma membrane wounding is considered the principal
mechano-sensing event that initiates the inflammatory response.
Tissue hypoxia associated with increasing fat mass may also play a role. Excess adiposity
increases the demand for oxygen to support tissue remodeling and vascularization. If the oxygen
demand of excess adipose tissue exceeds the oxygen supply, hypoxia could induce the
expression of genes such as hypoxia inducible factor-1a (HIF-1a) which triggers
cyclooxygenase-2 (COX-2) and the pro-inflammatory milieu observed with obesity.
Fat Cell Size, Number and Turnover in Humans
Investigations of human adipose tissue suggest that obesity is characterized by adipocyte
hypertrophy. In general, findings suggest that weight changes in adulthood are primarily due to
increases in adipocyte volume and size rather than number.
Nevertheless, approximately 10% of fat cells die and are replaced annually at all adult
ages and levels of body mass. Furthermore, neither adipocyte death nor generation rate is altered
in early obesity, suggesting that fat cell number is under tight genetic regulation.
Accordingly, individuals with a large number of fat cells may have a greater inherent fat
storage capacity than individuals with small numbers. It is therefore possible to categorize
obesity into two types: hypertrophic obesity (increased adipocyte volume) and hyperplastic
obesity (increased adipoctye number). Under normal conditions, the fat mass is therefore in a
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constant state of flux whereby the adipocyte number remains relatively constant.
Brown Adipose Tissue
While the role of white adipose tissue (WAT) is primarily that of energy storage and
homeostasis, brown adipose tissue (BAT) is principally involved in classic cold-induced nonshivering thermogenesis for the purpose of producing heat to help regulate body temperature.
Brown adipose tissue (BAT) is abundant in small mammals and hibernating animals and
constitutes about 5% of the body weight of human newborn infants. Its presence in newborns is
of great importance to avoid hypothermia. Brown fat is highly innervated and vascularized and
the cells have abundant mitochondria. Brown fat efficiently produces heat in response to signals
from the sympathetic nervous system. Brown fat diminishes rapidly during infancy and is
negligible in human adults. Adaptive thermogenesis and the dissipation of energy through heat
production are possible targets for obesity intervention.
Risk Factors of Obesity
The genesis of obesity is multifactorial involving both modifiable and non-modifiable
risk factors and determinants. For any individual, the development of obesity is a result of the
interaction of behavioral, environmental, socio-cultural, and genetic factors that collectively tip
the energy balance in favor of excess energy that is stored as fat.
The dramatic global rise in the prevalence of obesity during the past several decades
tends to rule out a genetic basis for the obesity epidemic on the rationale that, collectively, the
population gene pool could not have changed significantly in such a short period of time. The
obesity epidemic has therefore, more often been described as resulting from contemporary
“obesity-promoting” environmental factors interacting with relatively stable, but underlying
genes among those who are susceptible in the population. As a consequence, public health and
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health behavior research and intervention programs have focused primarily on the two
predominant behaviors that impact energy balance: dietary intake and physical activity.
In addition to the traditional perspective that energy excess leads to the subsequent
development of obesity, emerging factors which have generated interest as potential contributors
to the secular increase in obesity include genetic predisposition, demography (age, longevity,
gender, ethnicity), maternal influence during the perinatal period, psychological stressors (sleep
debt, emotional stress, depression), physiologic factors (adiposity rebound and fat cell
dynamics), food marketing strategies and food access, economic advances (urbanization,
automation and mechanization), organic pollutants (endocrine disruptors), assortative mating,
and pharmaceuticals that influence weight.
Genetics of Obesity
The marked increase in the prevalence of obesity in the last three decades has led some
investigators to question the importance of genetics in the etiology of obesity. Though it is well
established that obesity runs in families, family members tend to share similar environments and
behaviors in their patterns of diet and exercise. Furthermore, in the vast majority of families
studied, obesity does not segregate with a Mendelian pattern of inheritance. Still, the available
evidence clearly reflects significant genetic impact on measures of body mass and obesity. Three
genetic patterns are evident.
Monogenic forms of obesity are caused by single gene mutations that are extremely rare.
Examples include genetic deficiencies in key hormones that regulate appetite and metabolism
such as melanocortin and leptin
Syndromic forms of obesity, of which there are approximately 30 rare syndromes, arise
from discrete genetic defects or chromosomal abnormalities Such syndromes are often associated
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with mental impairment, dimorphic features and developmental abnormalities, e.g., Prader Willi
syndrome, Alstrom syndrome and Fragile X syndrome.
Polygenic forms of obesity occur as a result of the effects of multiple genes. Studies of
obesity in monozygous and dizygous twins, siblings, parents and their offspring, adoptees and
their adoptive parents, and extended pedigrees have consistently revealed a strong genetic and
heritable contribution to measures of adiposity, such as BMI, body fat, fat mass, and waist
circumference.
Notably, genetic studies conducted in different populations and environments have found
that 40% to 70% of the variability in body mass is “heritable”. Nevertheless, since human
genotypes cannot be replicated and studied in different environments, such studies are limited in
their ability to partition the variability due to genotype by environment interaction.
One explanation for the rapid rise in obesity is the mismatch between today’s
environment and "thrifty genes" that were selected for in the past under different environmental
conditions when food sources were rather unpredictable. This hypothesis was initially proposed
by geneticist James Neel to explain how genes predisposing to diabetes arose in the population.
According to the "thrifty genotype" hypothesis, the same genes that helped our ancestors survive
occasional famines are now being challenged by environments in which food is plentiful year
round.
Environmental Factors Contributing to Obesity
Environmental factors can increase the risk of developing obesity by directly or indirectly
influencing energy intake and energy expenditure. Two environmental factors have been
implicated as major culprits in causing obesity: food marketing strategies (especially to children)
and 24-hour availability of cheap, convenient, energy dense, high fat, high sugar, ultra-
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processed, super-sized, ready-to-eat meals, snacks, and drinks.
The trend of super-sized portions has been primarily economic and value-driven, with
consumers wanting “more food for their money” even choosing restaurants based on portion
sizes. Larger portion sizes equate to intake of more calories.
Environmental factors also influence physical activity levels and energy expenditure. For
example, the built environment, which reflects the land use and transportation patterns of a
population, can either facilitate or constrain physical activity. Urban sprawl patterns such as low
density land use, single use zoning, and employment dispersion may result in a heavy reliance on
motorized methods of transportation and lengthened commute times, as well as lack of
opportunities or spaces and places to walk, bicycle, and play safely. In addition, neighborhood
characteristics such a sidewalks, lighting, perception of safety, streetscapes, traffic calming
techniques, and other qualities may play a role in physical activity patterns, as well as
characteristics of parks, trails, and playgrounds.
Technological advances in the workplace, specifically mechanization and automation
have reduced physical activity requirements in almost all occupations and many technological
conveniences in the home have further reduced energy expenditure from daily living. While
energy expenditure from daily living has most certainly declined, so too has physical activity
requirements for school-age teenagers and children. For example, daily enrollment in physical
education classes has markedly declined among high school students and many public schools
have reduced or eliminated structured physically activity altogether. In addition to decreases in
physical activity, increased sedentary behaviors such as television viewing, computer use, and
playing video games have been linked to childhood adiposity.
Childhood Obesity
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Classification of Overweight and Obesity in Children and Adolescents
In the United States, childhood and adolescent overweight and obesity (ages 2-20 years)
are defined as the gender-specific 85th and 95th percentiles of Body Mass Index-for-Age, which
corresponds approximately to the respective BMI cut-off points of 25 and 30 for adults.
The Burden of Childhood Obesity
Globally, the number of overweight children under 5 years of age increased from 20
million in 2005 to 43 million in 2010. Though obesity rates are higher in developed countries, in
absolute numbers, developing countries have far more children that are obese. It is estimated that
there are 35 million overweight/obese preschoolers in developing countries compared with 8
million in developed countries.
In the United States, the steep rise in childhood obesity has paralleled the epidemic rise in
adult obesity. In 1990, the prevalence of childhood obesity did not exceed 15% in any state and
in ten states the prevalence was less than 10%. In sharp contrast, by 2008, only one state had a
prevalence of childhood obesity that was less than 20% and in 32 states, over a quarter of all
children were classified as obese.
Similar to the disproportionate burden of obesity observed among certain ethnic groups
of US adults, childhood obesity is more common among African Americans, Hispanics, and
American Indians compared to Caucasians. The distribution of childhood obesity also varies by
socioeconomic status. For instance, in a national survey of pre-school children aged 2-4 years,
the prevalence of obesity was highest among low-income children.
The risk of becoming an obese adult is much higher among children who are overweight
or obese compared to those who are not. Longitudinal studies clearly show that elevated BMI
tracks from childhood to adulthood, even after adjusting for parental obesity.
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Risk Factors in Early Life and the Development of Later Obesity
Perinatal Influences
Parent offspring studies suggest that maternal obesity, diabetes, malnutrition and other
psychological, immunological and pharmacological stressors during gestation can promote the
development of obesity in offspring. Postnatally, maternal diet and health, infant feeding
patterns, and adiposity rebound have all been associated with obesity in later life.
Early Adiposity Rebound and Future Health Risk
Adiposity rebound refers to the age at which the BMI reverses direction at its nadir
(lowest point) and increases towards adiposity. Studies have shown that early onset of adiposity
rebound (under 5 years of age) is related to obesity in later life, independent of parental obesity
and BMI at the time of the rebound.
Health Consequences of Childhood Obesity
The health consequences of obesity in children are similar to that observed in obese
adults, affecting multiple body systems. Obesity in children increases the risk of hypertension,
dyslipidemia, hyperglycemia, hyperinsulinemia, chronic inflammation, obstructive sleep apnea,
asthma, orthopedic complications, psychological distress, and psychosocial stigma.
Prevention of Obesity
Primary prevention of obesity and associated diseases begins in early life. The foundation
of successful obesity prevention programs is inclusion of effective dietary and physical activity
components. The dietary component should be designed to reduce energy intake and improve
nutritional content. The physical activity component should be designed to increase daily caloric
expenditure and decrease sedentary behavior. Periodic measures of weight, body mass, quality of
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life and other outcomes should be taken to gauge progress. Structured obesity prevention
programs and services may be offered in a variety of settings such as outpatient clinics, schools,
worksites, community centers, churches, fitness centers and neighborhood recreational facilities.
Therapy of Obesity
Therapeutic approaches to obesity include non-pharmacologic programs focused on diet
and exercise to reduce weight through manipulation of energy balance, and more recently,
administration of pharmacologic anti-obesity agents.
Liposuction
Liposuction refers to the suctioning of fat from certain areas of the body. The procedure
is performed primarily for cosmetic purposes. The value of liposuction in the treatment of
obesity is highly controversial. Additional investigations are needed to determine both the short
term and long term impact of high volume liposuction.
Bariatric Surgery
Although primary prevention is the best approach to attenuating the obesity epidemic and
controlling, improving, or reversing obesity-related co-morbidities, bariatric surgery is the only
proven treatment for severe obesity in adults and adolescents. Bariatric surgery is an elective
surgical weight loss procedure that reduces the gastric reservoir and limits food intake.
Summary
Obesity is dramatically increasing across the globe. Because of the profound rise in
obesity within the past several decades, most experts have ruled out a change in genetics as
contributing substantially to the obesity epidemic. Instead, increased urbanization worldwide is
leading to fundamental changes in physical activity levels and dietary patterns. Multiple
structural changes in the environment have led to decreased physical activity, increased
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sedentary behavior, and ready access to high fat, high sugar, energy dense, cheap food and drink,
and these changes have tipped the global energy balance scale so that long term energy intake
exceeds energy expenditure. Excess energy leads to an increase in energy stored as
triacylglycerol within adipocytes of white adipose tissue and subsequently excess weight gain.
Other risk factors include genetic susceptibility, female gender, aging, ethnicity, perinatal
factors (maternal obesity), menopause, psychological factors (stress, depression) and
physiological factors (adiposity rebound and fat cell dynamics). The rapid global rise in obesity
could at least in part be due to the mismatch between today’s environment and "thrifty genes"
that were selected for in the past under different environmental conditions when food sources
were unpredictable.
Obesity exerts deleterious effects on nearly every organ system of the body and is a
significant risk factor for type 2 diabetes, cardiovascular diseases (such as coronary heart
disease, myocardial infarction, and stroke), gastroesophageal reflux disease (GERD), obstructive
sleep apnea, asthma, gall bladder and fatty liver disease, depression, urinary incontinence, gout,
polycystic ovarian syndrome, and osteoarthritis. In particular, obesity promotes the parallel
progression of insulin resistance to type 2 diabetes and endothelial dysfunction to
atherosclerosis. Overall, obesity has become one of the leading causes of premature death and
disability in the world.
Adipocytes not only function as a storage repository for excess energy, but they also
actively participate in metabolic processes that regulate energy homeostasis. Excess adiposity
incites the synthesis of a multitude of autocrine, paracrine and endocrine bioactive signaling
proteins called adipokines. Certain adipokines (resistin and leptin) have pro-inflammatory
properties that promote atherogenesis and insulin resistance whereas others (adiponectin) are
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anti-inflammatory. Numerous studies indicate that visceral (abdominal) fat is more metabolically
active than subcutaneous (peripheral) fat, and that visceral adiposity is primarily responsible for
increasing the risk of developing obesity-related diseases.
Based upon studies of fat cell turnover, obesity can be classified into type basic types:
hypertrophic obesity (increased fat cell size) and hyperplastic obesity (increased fat cell number).
Preventive and therapeutic strategies should be designed to counteract both types.
As with adults, the prevalence of obesity in children has risen dramatically in populations
across the globe. Obesity in children increases the risk of hypertension, dyslipidemia,
hyperglycemia, hyperinsulinemia, chronic inflammation and many other health conditions.
Childhood obesity tracks to adult obesity, and early rebound adiposity is a significant predictor
of adult obesity.
While obesity is still increasing worldwide, recent US survey results indicate that the
epidemic may be abating in children, perhaps as a consequence of prevention programs in
schools and communities and public health awareness campaigns promoting a lifestyle of healthy
eating and regular exercise to maintain ideal body weight. Early health education is the
cornerstone of primary prevention. Clearly, comprehensive and sustainable prevention programs
should be established in populations around the globe to encourage healthy, nutritious eating
habits and physically active lifestyles in order to avoid the development of obesity and obesityrelated diseases in future generations.
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