Obesity: Causes and Consequences
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Description
Obesity results from a complex interplay of biologic, environmental, genetic, and psychosocial factors that influence appetite, satiety, and food storage in the form of body fat. At a fundamental level, obesity results from a sustained positive energy balance; that is, consuming more energy than one expends over an extended period of time. Weight gain results from excess caloric intake, and weight loss results from greater caloric expenditure than intake. Thus, excessive caloric intake and insufficient physical activity are the primary contributors to obesity.
Biologic Influences
Research has demonstrated that energy balance is highly influenced by a complex biological system. This system balances the amount of fat in the body, partially by regulating the unconscious drive to eat (Friedman, 2009). This drive to eat is adaptive in times of food scarcity but has become problematic given the relative abundance of high-calorie foods and limited physical activity participation in today’s society.
Genetic Contributors
Although the dramatic increase in obesity is not genetic in origin, genes interact with environmental factors to give individuals in the same environment significantly different risks of becoming obese. Estimates of the heritability of obesity – the percentage of variability due to genetic factors – range from 70% to 80%, indicating that genetics play a clear role in increasing one’s vulnerability to becoming obese (Walley, Asher, & Froguel, 2009).
Perinatal Influences
Recent research has also highlighted the important contribution of the perinatal environment to development of obesity. Studies have demonstrated that severely obese mothers are much more likely to have obese children than previously obese mothers who lost weight prior to conception (Kral et al., 2006). These results highlight the significance of gene-environment interactions: Epigenetic influences play a critical role in one’s likelihood of becoming obese.
Environmental Factors
There is increasing recognition of the extent to which environmental factors contribute to the rise in obesity. Indeed, American society has been characterized as an obesogenic environment that promotes excess eating and physical inactivity (Swinburn, Egger, & Raza, 1999). Energy expenditure has decreased for most individuals in the developed world, largely because employment primarily consists of sedentary work, energy-saving devices limit physical exertion, and transportation requires little physical effort. In concert with decreases in physical activity, access to highly palatable, inexpensive food that requires little or no preparation has increased dramatically. These foods are often high in caloric content and contain high amounts of fat and sugar. Additionally, the food industry promotes consumption of these foods through aggressive advertising and promotion, a practice that has been shown to increase their consumption (Kumanyika et al., 2008).
Research has consistently demonstrated that attributes of the “built” environment (i.e., buildings such as homes, schools, and shopping centers, as well as the ways in which these buildings are configured within space) also contributes to the prevalence of obesity. Individuals who live in walkable neighborhoods with access to recreation facilities are more likely to be physically active and less likely to be obese. Residents of communities with ready access to healthful foods tend to have healthier diets and lower incidence of obesity. Furthermore, environmental characteristics that contribute to obesity affect low-income and racial minorities disproportionately, contributing to higher levels of obesity among these groups (Sallis & Glanz, 2009). Fast-food restaurants in particular have been identified as a key contributor to the rise in obesity, and these restaurants are more prevalent in low-income neighborhoods, a characteristic thought to partially explain the higher incidence of obesity among the poor (Powell, Auld, Chaloupka, O’Malley, & Johnston, 2007).
Consequences of Obesity
A broad spectrum of medical, psychological, social, and behavioral consequences result from obesity. These consequences have been shown to arise from one of two factors: the increased mass of fat in the body of the obese individual and the risks resulting from metabolic changes associated with excess fat.
Consequences Due to Metabolic Changes
One of the most well-known risks associated with metabolic changes arising from excess fat is the higher incidence of type 2 diabetes mellitus. Associated conditions include insulin insensitivity and metabolic syndrome, a concurrence of elevated blood pressure, cholesterol, centrally deposited fat, and elevated blood sugar. Cardiovascular disease including hypertension is also a frequent consequence of obesity. Estimates suggest that as many as 50% of obese individuals suffer from hypertension. Excess body weight also increases the risk of heart failure. Increased cardiac work resulting from higher body mass raises the likelihood of cardiomyopathy and heart failure in obese individuals. Obese individuals are also at risk for nonalcoholic fatty liver disease, a constellation of liver abnormalities associated with obesity. Certain forms of cancer, including colorectal, prostate, and female reproductive and breast cancers, are more prevalent among obese individuals (Bray, 2004).
Consequences Due to Increased Fat Mass
Medical comorbidities associated with increased fat mass include osteoarthritis, cartilage and bone metabolism problems independent of weight bearing effects, and skin pigmentation and stretch marks. Obstructive sleep apnea risk is also greatly elevated in obese individuals.
Equally concerning are the psychosocial consequences associated with obesity. Obese individuals experience significant social stigmatization, including difficulty obtaining employment, education, and health care in addition to difficulties establishing and maintaining social relationships. Obese children are also more likely to have academic problems and to experience social difficulties, such as peer victimization and increased loneliness. Furthermore, obese individuals are more likely to report poor quality of life, depression, and disordered eating (Bean, Stewart, & Olbrisch, 2008).
Obesity Shortens Life
The detrimental effects of obesity combine to shorten life for individuals with this condition. Although estimates of life-shortening effects vary, obesity has been shown to shorten life on a population level. Indeed, the rise in rates of obesity has overwhelmed the positive effects of reduced rates of smoking on a population level (Stewart, Cutler, & Rosen, 2009). Individuals with obesity (BMI 30–39.9) have a reduced median survival rate of 2–4 years, while for those with extreme obesity (BMI 40–45), survival is reduced by 8–10 years (Prospective Studies Collaboration, 2009).
Conclusion
In summary, obesity is caused by energy imbalance resulting from excess caloric input relative to expenditure. The increased rate of obesity observed in the USA over the last three decades has been attributed primarily to an interaction between biologic risk for obesity and an obesogenic environment that provides limited opportunity for physical activity and ready access to calorie-dense foods. There are a number of medical and psychosocial consequences associated with obesity, including cardiovascular disease, joint problems, type 2 diabetes, depression, social stigmatization, poorer quality of life, and abbreviated life expectancy. These consequences underscore the importance of prevention and intervention efforts to ameliorate the negative consequences of obesity.
Cross-References
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