Obesity
Nancy A. Crimmins
Stavra A. Xanthakos
KEY WORDS
Bariatric surgery
Obesity
Overweight
Severely obese
Over the past 30 years, rising rates of obesity have occurred not only in the US, but also worldwide. Globally, obesity has nearly doubled since 1980, with nearly 11% of adults aged 20 and over estimated to be obese in 2008. Overweight and obesity are the fifth leading cause for global deaths, causing an estimated 2.8 million annual deaths in adults. Within the US, more than one-third of adults (age-adjusted 34.9%) are now obese based on the most recent national health surveys in 2011 to 2012.1 Although the rate of obesity is slightly lower in younger adults aged 20 to 39, it remains strikingly high at 30.3%.2 In adolescents, rates of obesity quadrupled from 5.0% in 1980 to 20.5% in 2011 to 2012.3 The prevalence in emerging young adults aged 20 to 24 has gone up from 24.1% to 28.7% from 2001-2002 to 2007-2008 with significant worsening in this population and rates significantly worse than adolescents.4 Health care providers who care for adolescents and young adults (AYAs) will encounter a substantial number of affected young people with obesity. As such, they need to be prepared to accurately diagnose obesity and the related health problems and counsel on appropriate prevention and treatment options for this age group.
DEFINING OVERWEIGHT AND OBESITY IN AYASBody mass index (BMI), a simple index of weight-for-height (kg/m2), is the most commonly used and recommended tool to screen for excess adiposity at all ages. Adult overweight is defined as a BMI of ≥25 kg/m2 and adult obesity as a BMI of ≥30 kg/m2. However, using a set BMI cut-point in adolescents is not feasible due to growth-related changes in weight and height. Therefore, age- and gender-specific BMI percentile distributions in the Centers for Disease Control and Prevention (CDC) growth charts are the preferred reference (www.cdc.gov/growthcharts/).
Adolescent Obesity
Overweight
Overweight is defined as a BMI of ≥85th percentile for age and gender, but less than the 95th percentile or 30 kg/m2 (whichever is lower).
Severely Obese
Approximately 4% to 6% of all youth in the US have been recognized as “severely obese.” These youth carry a much higher burden of cardio-metabolic risk factors and have a propensity to remain severely obese into adulthood. In the Bogalusa Heart Study, severely obese youth (defined as ≥99th percentile for age and gender) had a nearly five-fold increase (33% versus 7%) of having three or more cardiovascular risk factors compared to those at the 95th percentile.7 In addition, 100% of these youth remained obese as adults, with 88% still severely obese as adults (BMI ≥ 35 kg/m2).7 The current recommended definition for extreme pediatric obesity is a BMI of 120% or 1.2 × the 95th percentile BMI or a BMI of ≥35 kg/m2 (whichever is lower).8 Of note, a BMI of 35 kg/m2 is higher for most youth, except for boys approximately18 years of age and girls ≥16 years.
BMI
BMI is a very useful screening tool but has limitations. A high BMI may reflect a larger fat-free mass in very athletic AYAs with high muscle mass.9 There are also racial and ethnic differences in percentages of body fat at the same BMI, with Mexican American and South Asian children having higher percentages and African-American children lower percentages of body fat than children of White European heritage.10 However, at this time, the same BMI reference percentiles are currently recommended for all US youth. Skin-fold thickness and waist circumference have also been used to measure and track excess adiposity using percentile cutoffs.11 These methods are not currently recommended for routine clinical use, as they require specific training to perform accurately and consistently.5
EPIDEMIOLOGY OF OBESITY IN AYAsData from national health surveys performed between 1976 and 2012 show that the prevalence of obesity in 12- to 19-year-olds of both genders has essentially quadrupled from 1997-1980 to the present 2011-2012 survey12,13 (Table 32.1). Data from 2011 to 2012 show a 20.5% prevalence of obesity among adolescents 12 to 19 years of age, with a prevalence of 20.3% in males and 20.7% in females.3 The prevalence of obesity among young adults aged 20 to 24 is even higher at 28.7%.4 There has been a relative plateau in obesity prevalence among all children and adolescents since 2003 to 2004.3 However, disparities in obesity rates remain among ethnic and racial groups, with Hispanic youth and non-Hispanic Black youth having the highest prevalence rates, followed closely by non-Hispanic White youth, while non-Hispanic Asian youth have the lowest rates (Table 32.1).
Despite an overall plateau in pediatric obesity, there has been a continued rise in severe obesity regardless of the definition used (see above).8 This may portend a substantial rise in morbidity and
mortality in our next generation of young adults, given the higher number of cardiovascular risk factors and likelihood to remain severely obese as adults.7 Severe obesity at age 18 years is associated with a significant increased risk of premature death in adulthood with a hazard ratio for death from all causes of 2.46 (95% confidence interval (CI), 1.91, 3.16) for severely obese and 1.41 (95% CI, 1.15, 1.73) for those obese at age 18 compared to those of normal weight.14
mortality in our next generation of young adults, given the higher number of cardiovascular risk factors and likelihood to remain severely obese as adults.7 Severe obesity at age 18 years is associated with a significant increased risk of premature death in adulthood with a hazard ratio for death from all causes of 2.46 (95% confidence interval (CI), 1.91, 3.16) for severely obese and 1.41 (95% CI, 1.15, 1.73) for those obese at age 18 compared to those of normal weight.14
TABLE 32.1 Obesity Prevalence in Adolescents Aged 12 to 19 Years (US National Health and Nutrition Examination Surveys) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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CAUSES OF OBESITYObesity is a complex condition influenced by multiple intrinsic and extrinsic risk factors, ultimately contributing to a fundamental imbalance between calories consumed and calories expended.
Environmental and Behavioral Risk Factors
Major societal changes over the past century have likely played the greatest role in our current epidemic of obesity. These include:
Improvements in food production and government subsidies resulting in greater availability of cheaper energy-dense (and frequently nutrient-poor) foods high in sugar and fat.
Decrease in home-cooked family meals and greater reliance on commercially prepared foods, in part due to more dual wage-earner families. Processed food products are often specifically designed by manufacturers to be intensely appealing to natural human taste preferences for sweet, salty, and fatty foods.
Concurrent technological advances that have dramatically reduced energy expenditure in both work and leisure-time activities. Television and computer gaming devices are ubiquitous in the homes and bedrooms of many AYAs. This not only contributes to increased sedentary behavior, but may result in reduced sleep duration, which has been linked to increased food intake.15,16
Familial or Genetic Risk Factors
Weight is a heritable trait. The concordance of fat mass in monozygotic twins ranges from 70% to 90% compared to 35% to 45% in dizygotic twins.17 Furthermore, adoption studies have shown a much stronger correlation of BMI with the adoptee’s biological parents compared to their adoptive parents.17 However, the specific genes involved have proven difficult to isolate and replicate in genome-wide association studies.
Monogenic mutations: Monogenic mutations are a rare cause of obesity. The most common is a mutation in melanocortin-4 receptor (MC4R), which leads to alterations in leptin-melanocortin signaling and loss of satiety. The prevalence of MC4R mutations in obese children ranges from 0.5% to 5.8%,18 with clinical onset of obesity by age 2 years. Mutations in the LEP and LEPR can also lead to early-onset obesity, as well as hyperphagia, delayed puberty, and immune dysfunction. Although true leptin deficiency is rare, mutations in LEPR were found to have a prevalence of 3% in a cohort of early-onset obesity and hyperphagia.19 Leptin levels in individuals with leptin receptor mutations are elevated; however, levels can also be elevated due to the leptin resistance frequently seen in patients with obesity and insulin resistance. Therefore, measuring leptin concentrations alone cannot diagnose mutations in the receptor and genetic analysis must be performed to diagnose mutations.
Other genes: Other genes implicated in the development of obesity include genes in the melanocortin-leptin signaling system (proopiomelanocortin, melanocortin 2-receptor); brain-derived neurotropic factor (BDNF) and its receptor tyrosine receptor kinase B; and the fat mass and obesity-associated (FTO) gene. Genetic syndromes associated with obesity include Prader-Willi, Bardet-Biedl, and Alstrom syndromes. AYAs with developmental delay, dysmorphic features, or organ dysfunction should be referred to a genetics specialist for evaluation to rule out syndromes with obesity as a component.Related posts:
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