126 Obesity
expenditures in the United States. The indirect costs (i.e., lost
productivity due to morbidity and mortality from diseases as-
sociated with obesity) amount to an additional $47.6 billion.
In addition, consumers spend in excess of $33 billion annu-
ally for weight-loss interventions, exercise programs, weight-
control books, and diet foods and beverages (Thomas, 1995).
Researchers estimate that the overall economic impact of
obesity is similar to that of cigarette smoking (NHLBI, 1998;
Wolf & Colditz, 1998).
CONTRIBUTORS TO OBESITY
Given the prevalence and seriousness of obesity, it is essen-
tial that we understand its etiology. Understanding the factors
that contribute to the development of obesity may lead to ef-
fective interventions for its control and prevention. In this
section, we address genetic and environmental contributors
to overweight and obesity.
Genetic Contributors
In the past decade, there has been great enthusiasm about the
prospects of identifying the biological causes of obesity. A
body of research showing that obesity tends to run in families
spurred the search for the genetic basis of obesity. For exam-
ple, familial studies consistently have shown that BMI is
highly correlated among “rst-degree relatives (Bouchard,
Perusse, Leblanc, Tremblay, & Theriault, 1988), and investi-
gations of identical twins reared apart have suggested that
the genetic contribution to BMI may be as high as 70%
(Stunkard, Harris, Pedersen, & McClearn, 1990). Such “nd-
ings have led researchers to suspect that a single major, but as
yet unidenti“ed, recessive gene accounts for a signi“cant
proportion of the variance in body mass (Bouchard, Perusse,
Rice, & Rao, 1998). In addition, researchers also believe that
body-fat distribution, resting metabolic rate, and weight gain
in response to overconsumption are each controlled by ge-
netic factors that may interact to predispose certain individu-
als to obesity (Chagnon et al., 2000; Feitosa et al., 2000;
Levin, 2000).
Among the “rst genetic defects linked to obesity was the
discovery of the ob gene and its protein product leptin (Zhang
et al., 1994). Leptin, a hormone produced by fat cells, in”u-
ences hypothalamic regulation of energy intake and expendi-
ture. Laboratory mice that fail to produce leptin due to a
genetic defect become obese as the result of excess energy in-
take and physical inactivity (Zhang et al., 1994). Moreover,
the administration of recombinant leptin in such animals de-
creases food intake, increases physical activity, and reduces
body weight (Camp“eld, Smith, Guisez, Devos, & Burn,
1995). In humans, however, only a very small percentage of
obese individuals have leptin de“ciencies (Montague et al.,
1997). Most obese individuals actually have higherrather
than lower levels of leptin due to their higher levels of adi-
pose tissue (Considine et al., 1996). Thus, some researchers
(Ahima & Flier, 2000) have suggested that obese persons
may become leptin •resistantŽ similar to the way obese per-
sons with type 2 diabetes become insulin resistant. Trials of
recombinant leptin as treatment for obesity have yielded
modest results. High doses of leptin (administered via daily
subcutaneous injections) have produced reductions in body
weight of about 8%„a decrease equivalent to what is typi-
cally accomplished in lifestyle interventions (Heyms“eld
et al., 1999).
Several other single-gene defects have been discovered
that contribute to obesity in animals (Collier et al., 2000;
Levin, 2000). However, only one of these mutations appears
to be a frequent contributor to human obesity. Investigators
(Farooqi et al., 2000; Vaisse et al., 2000) have found that 4%
of morbidly obese individuals display a genetic mutation in
the melanocortin-4 receptor (MC4), which plays a key role
in the hypothalamic control of food intake. Thus, research
into the MC4 receptor and other potential genetic causes of
obesity continues at a rapid pace (Comuzzie & Allison, 1998).Environmental ContributorsPoston and Foreyt (1999) have recently argued that •genes
are not the answerŽ to understanding the development of obe-
sity (p. 201). They maintain that animal models of obesity are
severely limited in their generalizability to humans. More-
over, they contend that several sources of information indi-
cate that environmental factors are the primary determinants
of human obesity.
For example, the in”uence of sociocultural factors on the
development of obesity can be seen in preindustrialized soci-
eties that undergo a transition to modernization (i.e., West-
ernization). In a classic study of the association between
obesity and modernization in Polynesia, Prior (1971) found
that the prevalence of obesity in the highly Westernized re-
gion of Maori was more than double the rate of obesity on the
more traditional island of Pakupaku (i.e., 35% versus 15%,
respectively). Similarly, the in”uence of environmental fac-
tors can be seen in a comparison of groups that share the
same genetic heritage but live in environments that support
very different lifestyles. For example, the Pima Indians of
Arizona, who live in a •modernŽ environment, have the high-
est prevalence of obesity of any ethnic/racial group in the
United States (Krosnick, 2000). However, the prevalence of