Obesity: Responding to the global epidemic.

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Abstract

Obesity has reached epidemic proportions in the United States and other developed nations. In the United States, 27% of adults are obese and an additional 34% are overweight. Research in the past decade has shown that genetic influences clearly predispose some individuals to obesity. The marked increase in prevalence, however, appears to be attributable to a toxic environment that implicitly discourages physical activity while explicitly encouraging the consumption of supersized portions of high-fat, high-sugar foods. Management of the obesity epidemic will require a two-pronged approach. First, better treatments, including behavioral, pharmacologic, and surgical interventions, are needed for individuals who are already obese. The second and potentially more promising approach is to prevent the development of obesity by tackling the toxic environment. This will require bold public policy initiatives such as regulating food advertising directed at children. The authors call not for the adoption of a specific policy initiative, but instead propose that policy research, based on viewing obesity as a public health problem, become a central focus of research.

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Most cited references 113

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Environmental contributions to the obesity epidemic.

J Hill, J Peters (1998)

The current epidemic of obesity is caused largely by an environment that promotes excessive food intake and discourages physical activity. Although humans have evolved excellent physiological mechanisms to defend against body weight loss, they have only weak physiological mechanisms to defend against body weight gain when food is abundant. Control of portion size, consumption of a diet low in fat and energy density, and regular physical activity are behaviors that protect against obesity, but it is becoming difficult to adopt and maintain these behaviors in the current environment. Because obesity is difficult to treat, public health efforts need to be directed toward prevention.

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Physical fitness and all-cause mortality. A prospective study of healthy men and women.

S N Blair, H W Kohl, R S Paffenbarger … (1989)

We studied physical fitness and risk of all-cause and cause-specific mortality in 10,224 men and 3120 women who were given a preventive medical examination. Physical fitness was measured by a maximal treadmill exercise test. Average follow-up was slightly more than 8 years, for a total of 110,482 person-years of observation. There were 240 deaths in men and 43 deaths in women. Age-adjusted all-cause mortality rates declined across physical fitness quintiles from 64.0 per 10,000 person-years in the least-fit men to 18.6 per 10,000 person-years in the most-fit men (slope, -4.5). Corresponding values for women were 39.5 per 10,000 person-years to 8.5 per 10,000 person-years (slope, -5.5). These trends remained after statistical adjustment for age, smoking habit, cholesterol level, systolic blood pressure, fasting blood glucose level, parental history of coronary heart disease, and follow-up interval. Lower mortality rates in higher fitness categories also were seen for cardiovascular disease and cancer of combined sites. Attributable risk estimates for all-cause mortality indicated that low physical fitness was an important risk factor in both men and women. Higher levels of physical fitness appear to delay all-cause mortality primarily due to lowered rates of cardiovascular disease and cancer.

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Long-term morbidity and mortality of overweight adolescents. A follow-up of the Harvard Growth Study of 1922 to 1935.

A Must, P Jacques, G Dallal … (1992)

Overweight in adults is associated with increased morbidity and mortality. In contrast, the long-term effect of overweight in adolescence on morbidity and mortality is not known. We studied the relation between overweight and morbidity and mortality in 508 lean or overweight adolescents 13 to 18 years old who participated in the Harvard Growth Study of 1922 to 1935. Overweight adolescents were defined as those with a body-mass index that on two occasions was greater than the 75th percentile in subjects of the same age and sex in a large national survey. Lean adolescents were defined as those with a body-mass index between the 25th and 50th percentiles. Subjects who were still alive were interviewed in 1988 to obtain information about their medical history, weight, functional capacity, and other risk factors. For those who had died, information on the cause of death was obtained from death certificates. Overweight in adolescent subjects was associated with an increased risk of mortality from all causes and disease-specific mortality among men, but not among women. The relative risks among men were 1.8 (95 percent confidence interval, 1.2 to 2.7; P = 0.004) for mortality from all causes and 2.3 (95 percent confidence interval, 1.4 to 4.1; P = 0.002) for mortality from coronary heart disease. The risk of morbidity from coronary heart disease and atherosclerosis was increased among men and women who had been overweight in adolescence. The risk of colorectal cancer and gout was increased among men and the risk of arthritis was increased among women who had been overweight in adolescence. Overweight in adolescence was a more powerful predictor of these risks than overweight in adulthood. Overweight in adolescence predicted a broad range of adverse health effects that were independent of adult weight after 55 years of follow-up.