Though the scientific community has been unable to identify a single etiologic agent for obesity, there have been clinical advances in the past two decades. Obesity is known to be associated with certain exogenous causes. Genetic factors gained national attention after the discovery of leptin in 1995 by positional cloning in the leptin-deficient mouse model of obesity [19]. Leptin (derived from the Greek word leptos, meaning “thin”) is a 16-kilodalton adipocyte-derived hormone from the ob gene and has been the focus of many genetic investigations to elucidate the pathophysiology of obesity. Though this finding is relatively recent, its existence was suspected twenty years ago. In 1978, Coleman proposed that a circulating factor in the plasma of the db mouse strain, which is both diabetic and obese, could reduce the obesity of the ob mouse (a strain of mice with mutations in leptin) [20]. The db mice were found to have mutations in the leptin receptor and were subsequently resistant to the leptin, unlike the ob mice who possessed a mutated leptin gene but functional leptin receptors. Further investigations revealed that injections of leptin in ob mice could cure obesity and diabetes. After locating the human homologues to the leptin gene and its receptor in 1999, the chromosomal locus containing the leptin gene was determined to be genetically related to human body weight [21]. However, only a few people with mutated leptin genes have been identified, while the majority of obese patients have fully functional leptin genes and receptors.
Genetic diseases with associated obesity include Schinzel syndrome, Bardet-Biedel syndrome, Albright hereditary osteodystrophy, and Prader-Willi syndrome. Many of these genetic disorders present with dysmorphic features, developmental delay, and obesity in addition to changes seen specifically with each disorder [22]. For instance, young males with Prader-Willi syndrome present with the features described above as well as with linear growth defects and undescended testicles.
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Overall, the relationship between genetics and obesity cannot be fully determined at this time. Evidence suggests a link between the two, implying that genetics is one of the complex factors involved in the development of this prevalent condition. Although many argue that “obesity genes” cannot be responsible for the epidemic, because the gene pool in the United States had not changed significantly between 1980 and 1994, the etiology of obesity is most likely multifactorial [23]. In 2010, one group of researchers confirmed 14 genetic variations and discovered an additional 18 variations associated with obesity [77]. In 2015, the group published additional research that identified a total of 97 genetic variations [111]. Although the progress with genetic variations related to BMI is promising, further research is needed to clarify the influence of genetics.
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Biologic factors must also be considered. Proteins and receptors appear to have a role in weight control. For example, orexin A and B are located in the lateral hypothalamus, an area which may regulate body weight. Ongoing research may help determine the role of orexin in obesity.
Environmental factors seem to play a significant role as well. Data from a longitudinal twin-family study and co-twin control studies combined with population-based data on patterns of dietary intake and physical activity provide some evidence that environment can contribute to obesity [74]. Environmental factors include technologic advances in food processing, marketing, advertising, and behavioral lifestyle. Some theorize that obesity is self-fulfilling in that if an individual is told they are predisposed to becoming fat, he or she will decide there is no point in eating healthy or exercising [78].
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