The human life expectancy has steadily increased over the past few centuries; however, the current generation may be the first with a shorter life expectancy than their parents. The reason behind this unfortunate reversal is not increasing cancer rates or development of resistant bugs or new viruses, but a global increase in obesity and associated comorbidities.¹

Obesity is defined as an excess accumulation of body fat and is commonly defined as a body mass index (BMI) of >30 kg/m². In the United States, obesity affects 40% of women, 35% of men, and 17% of children and adolescents. In 2014, there were 600 million obese patients worldwide, with several countries having obesity rates greater than those in the United States. The highest rates of obesity can be found in some of the Pacific Island nations where obesity rates are greater than 40%. Obesity has been classified into several subcategories, as summarized in Table 36-1, with estimated prevalences from the National Health and Nutrition Examination Survey (NHANES) 2013 to 2014 data.² Severe obesity is often regarded as BMI ≥40, or ≥35 with obesity-related comorbidities. Superobesity is defined as a BMI ≥50.

With the growing obesity epidemic, there has also been an increase in the prevalence of morbid obesity over the past decade, with a linear growth in the rate of morbid obesity in women.

Although BMI is easy to calculate and has become the universally accepted measure for defining and classifying obesity, it is not ideal and has several limitations because it does not directly measure excess fat accumulation. As a result, a 70-inch muscular and fit athlete who weighs 215 pounds and has a BMI of 31 will be regarded as obese even though they have little excess fat accumulation. Although one can define obesity as percent body fat >32% in women and >25% in men, these calculations are difficult. More importantly, neither BMI nor percent body fat calculations provide any information on the regional body fat distribution. This is important because intra-abdominal and visceral obesity is associated with greater risk of insulin resistance, hyperlipidemia, hypertension, cardiovascular disease (CVD), and stroke than peripheral fat distribution. This difference is important because those with central obesity (android or apple pattern of obesity) have a greater risk of diabetes and CVD than those with fat accumulation in the subcutaneous tissue of buttock areas (gynoid or pear pattern of obesity). This difference in fat distribution may explain why individuals of Asian origin have a greater risk of diabetes at a lower BMI.³ As a result, many have proposed lowering the BMI threshold at which weight management interventions, including surgery, are recommended in this population group.

The global epidemic of obesity is multifactorial and has genetic, environmental, and epigenetic roots. It is thought that the recent exposure of man to an environment with excess and readily available food leads to an imbalance between caloric intake and energy expenditure, resulting in excess fat deposition. The reduction in physical activity and our new sedentary lifestyle have a significant role to play in the current obesity epidemic. Obesity is strongly and inversely related to degree of moderate physical activity, with small changes in daily levels of moderately vigorous physical activity leading to large differences in risk of obesity. Of all sedentary behaviors, prolonged television (TV) watching appears to be the most predictive of obesity and diabetes risk. In the Nurses’ Health Study, after adjustment for age, smoking, exercise level, and dietary factors, every 2-hour increment spent watching TV was associated with a 23% increase in obesity and a 14% increase in the risk of diabetes.⁴ The detrimental effect of TV on weight is in large part due to frequent snacking while watching TV and the associated increase in calorie intake, rather than decrease in physical activity alone.

Many studies have also confirmed that genetic factors influence obesity. In a meta-analysis of genomewide association studies (GWAS) and Metabochip studies involving nearly 34,000 patients, 97 loci were identified that were associated with BMI and accounted for approximately 2.7% of BMI variation. The GWAS analysis suggested that common variation accounts for about 21% of BMI variation.⁵ Thus, although in rare cases such as leptin deficiency, a genetic mutation may be the primary factor in the development of obesity, the more common situation is where susceptibility genes interact with environmental factors to predispose individuals to obesity.⁶ As an example, in a recent study of nearly 9000 people, the association between BMI and a polygenic risk score was higher in recent birth cohorts compared with earlier birth cohorts, likely due to the earlier exposure of the more recent cohort to our “obesogenic” environment.⁷

Although there is ongoing debate as to the etiology of the current obesity epidemic, there is little doubt over its adverse impact on health, quality of life, and life expectancy, with individuals who have a BMI >40 having a reduced life expectancy of 8 years. The adverse effect of obesity on mortality rate has been confirmed in differing population cohorts across the world where each 5-unit increase in BMI increased mortality rate by 39% in Europe, 29% in North America, 39% in East Asia, and 31% in Australia and New Zealand. For the 4 populations combined, all-cause mortality risk increased with increasing BMI when compared to individuals with a BMI between 22.5 and 25 as baseline: 7% for BMI of 25.0 to <27.5, 20% for BMI of 27.5 to <30.0, 45% for BMI of 30.0 to <35.0, and 94% for BMI of 35.0 to <40.0.⁸

The increase in mortality in obese individuals is due to increased risk of many serious and chronic conditions including type 2 diabetes, heart disease, hypertension, stroke, hyperlipidemia, cancer, and sleep apnea (Table 36-2). The prevalence of these comorbidities often increases even with modest further weight gain. This observation is most striking when looking at type 2 diabetes. Compared with women with stable weight and after adjusting for age and BMI, the relative risk for diabetes mellitus increased 2-fold in women who had a weight gain of 5.0 to 7.9 kg and increased by 3-fold in those who gained 8.0 to 10.9 kg.^9,10

Metabolic Syndrome

The observation that central obesity, with or without excess total body weight, and associated hypertension, hyperlipidemia, and insulin resistance can increase risk of CVD and diabetes suggested the existence of a “metabolic syndrome.” This syndrome has also been known as syndrome X or obesity dyslipidemia syndrome. Several differing definitions have been used for this condition, as summarized in Table 36-3.¹¹

The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) definition of metabolic syndrome is the most widely used, whereas the International Diabetes Federation (IDF) defines it as increased waist circumference, with ethnic-specific waist circumference cut points (Table 36-4).