The prevalence of obesity has risen dramatically in recent decades due to numerous interrelated factors. Increased caloric intake from highly processed, affordable, and accessible foods has contributed, as has decreased energy expenditure due to declining physical activity. Other contributors include changes in sleep patterns, medication use, smoking rates, environmental pollutants, urban design, and social networks. Genetics also play a role through their interaction with lifestyle and environmental conditions. Reversing obesity will require interventions that address its complex, multifactorial causes at both societal and individual levels.

1. Causes of obesity
Suzanne M. Wright, Louis J. Aronne
Comprehensive Weight ControlProgram, Weill-Cornell Medical College/New York Presbyterian Hospital, 1165 York
Avenue, New York, NY 10065, USA DOI:10.1007/s00261-012-9862-x Publishedonline: 18 March 2012
The prevalence of obesity has been rising steadily over the last several decades
and is currently at unprecedented levels: more than 68% of US adults are considered
overweight, and 35% are obese (Flegal et al., 2010). This increase has occurred
across every age, sex, race, and smoking status, and data indicate that segments of
individuals in the highest weight categories (i.e., BMI > 40 kg/m2) have increased
proportionately more than those in lower BMI categories (BMI < 35 kg/m2). The
dramatic rise in obesity has also occurred in many other countries, and the causes of
this increase are not fully understood (Hill and Melanson, 1999). Although obesity is
most commonly caused by excess energy consumption (dietary intake) relative to
energy expenditure (energy loss via metabolic and physical activity), the etiology of
obesity is highly complex and includes genetic, physiologic, environmental,
psychological, social, economic, and even political factors that interact in varying
degrees to promote the development of obesity (Aronne, Nelinson, and Lillo, 2009).
The food, or ‘‘built’’ environment has shifted in ways that promote overeating: highly
caloric and fat-laden foods are not only affordable but also easily accessible (i.e.,
numerous fast food restaurants, vending machines of energy dense items in schools
and offices, etc.). These highly palatable foods are frequently available in large
portions, which contribute to increased daily caloric intake (Rolls, 2003). Not only have
commercial portion sizes increased, the number of processed food items (typically
high in sugar, fat, and sodium) available in grocery stores, mini-marts, and
convenience stores has skyrocketed. Today, the majority of products in grocery stores
are non-perishable, highly processed, and pre-packaged foods. These products are
heavily marketed not only to adults but also to children as well. Convenient, easy to
prepare, and inexpensive, these high calorie products are frequently consumed by
millions of families who are struggling to meet the economic and scheduling demands
of today’s fast paced lifestyle.
Physical activity levels have also dramatically decreased in the past several
decades. It has been estimated that less than half of US adults engaged in
recommended levels of physical activity in 2005 (Centers for Disease Control and
Prevention, 2007). Levels of physical activity have also decreased in adolescents
(Kimm, 2002). There is less access to physical activity (fewer sidewalks), less physical
education in schools (Gabbard, 2001), and more time is spent on sedentary behaviors
such as television watching, surfing the internet, and playing video games (Andersen,
1998). The myriad advances in technology developed over the past few decades have
made many tasks more efficient, but in the process have ultimately decreased the
number of calories expended (i.e., TV remote controls, automatic garage door opener,
etc.).

2. In addition to the primary influences of increased caloric intake and decreased
energy expenditure, Keith et al. (2006) identified ten other contributing factors to the
obesity epidemic (Table 1). Weight gain is associated with several commonly used
medications including psychotropic medications, diabetic treatments, antihyper
tensives, steroid hormones and contraceptives, antihistamines, and protease
inhibitors. The deleterious effects of drug-induced weight gain include, paradoxically,
increased risks for developing type II diabetes, hypertension, hyperlipidemia, as well
as poor medication compliance (Aronne and Segal, 2003). While it is difficult to
estimate the full impact of drug-induced weight gain, the recognition that some of the
most widely prescribed classes of drugs can cause significant weight gain supports
the hypothesis that drug-induced weight gain is contributing to the obesity epidemic.
Table 1. Contributing Factors to the Obesity Epidemic
Contributingfactor References
The foodenvironment (Rolls, 2003)
Decreases in physical activity (Centers forDisease Control andPrevention, 2007)
Sleep debt (Gangwisch, 2005)
Drug-inducedweight gain (Aronne,2003)
Decline in cigarette smoking (Filozof et al.,2004)
Endocrine disruptors (Pelletieret al., 2003)
Reduction in variabilityof ambient temperature (Collin et al., 2001)
Changes in distribution ofethnicityandage (Hedley et al., 2004)
Increasinggravida age (Patterson, 1997)
Intrauterine effects (Finch andLoehlin,1998)
Greater reproductive fitness of higher BMIindividuals yieldingthe selectionfor
obesity-predisposinggenotypes
(Segal andAllison, 2002)
Assortative matingandflooreffects (Katzmarzyk et al., 2002)
Changes in policy (Swinburn et al., 2011)
Infections (Atkinson,et al.,2005)
Modified from [9, 19]
Sleep debt has also been linked to increased body weight. Some studies have
shown that hours of sleep per night are negatively correlated with BMI (Gangwisch et
al., 2005), and sleep restriction has been shown to increase hunger and appetite
(Spiegel et al., 2004). The relatively recent decline in cigarette smoking may also be a
factor that has contributed to the obesity epidemic, since studies have shown that
weight gain is a common sequelae of smoking cessation. Furthermore, smokers
typically weigh less than non-smokers.
Endocrine disruptors, industrially produced substances that can affect endocrine
function, may also be a contributing factor to the etiology of obesity. They include
dichlorodiphenyltrichloroethane, some polychlorinated biphenols and some
alkylphenols, that may act by disturbing endogenous hormonal regulation (Keith et al.,
2006). Other factors (Table 1) that can possibly contribute to the obesity epidemic
include a reduction in the variability of ambient temperature due to central cooling and
heating, changes in population distribution of ethnicity and age, increasing gravida
age, intrauterine effects, and greater reproductive fitness of higher BMI individuals

3. yielding the selection for obesity-predisposing genotypes. Although the genetics of
obesity is a highly researched area, just a small number of rare single genetic
abnormalities have been discovered. Current research on the epigenetics of obesity is
investigating the influence of behavioral and environmental factors on genetic
expression (Swinburn et al., 2011).
It has been suggested that policies put into place by the US government to increase
the food supply in the 1970s contributed to an abundance of food and therefore an
increase in population energy intake (Swinburn et al., 2009). For instance, US farm
subsidy policies may have caused certain foods to be more abundant and cheaper,
potentially contributing to lower relative prices and increased consumption of fattening
foods (Wallinga, 2010). Infections may also play a role in the etiology of obesity.
Adenovirus-36 (Ad-36) infection has been shown to cause obesity in animals (Pasarica
et al., 2006) and studies have shown that obese individuals are more likely to have
been infected with Ad-36 (Atkinson et al., 2005)
Social networks may also contribute to the increasing prevalence of obesity. One
study showed that a person’s chance of becoming obese increased by 57% if he or
she had a friend who became obese in a given interval (Christakis and Fowler, 2007).
A similar phenomenon was observed among adult siblings and married couples.
Among adult siblings, the chance of one sibling becoming obese increased by 40% if
the other sibling had become obese, and among married couples, the likelihood of one
spouse becoming obese increased by 37% if the other had become obese.
Thus, the dramatic rise in the incidence of obesity in many countries appears to be
due to the complex interaction of a variety of factors including genetic, physiologic,
environmental, psychological, social, economic, and political. Given the numerous and
significant deleterious health consequences associated with obesity, there is an urgent
need for the development of highly effective interventions that aim to reverse these
‘‘obesogenic’’ drivers, including both government policies as well as health education
and promotion programs.

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