Obesity is defined according to the body mass index (BMI), calculated by dividing weight in kilograms by height in meters squared. When this number is 30 or higher, an individual is considered to have obesity (Table 11). A number of organizations have supported the classification of obesity as a disease45-47 and in June 2013, an American Medical Association (AMA) policy resolution recognizing obesity as a disease requiring a range of medical interventions was officially adopted.48
|Classification||BMI, kg/m2||Risk of comorbidities|
|Underweight||< 18.5||Low, but increased risk of other clinical problems|
|Obesity (Grade 1)||30–34.9||Moderate|
|Obesity (Grade 2)||35–39.9||Severe|
|Obesity (Grade 3)||≥ 40||Very severe|
In children older than 2 years of age, obesity is defined as a BMI at or above the 95th percentile of the 2000 CDC sex-specific BMI-for-age growth charts.51,52 While there is no standard definition of obesity for children younger than age 2 years, recent analyses have used weight for recumbent length at or above the 95th percentile on the CDC sex-specific weight for recumbent length growth charts (Table 12).2,53
|Classification||Weight as a Percentile of height|
|Underweight||< 5th percentile|
|Normal weight||5th to 85th percentile|
|Overweight||85th to 95th percentile|
|Obesity||> 95th percentile|
Source: Ogden and Flegal, 201052
It is recognized that universal BMI values used to define obesity may not be appropriate for all populations based on factors such as age, sex, race and ethnicity.54 For example, persons of Asian descent may have different body fat levels at the same BMI. Although a technical review by the World Health Organization and the ACC/AHA/TOS Guidelines both recommended that universal BMI ranges be retained as an international classification, they suggested the possibility of revised thresholds for Asian populations as trigger points for public health action.55 Additional measures such as waist circumference may also offer better indicators of morbidity and mortality risk in such populations.56
The latest prevalence data shows that over one in three adults has obesity. Among the various age groups, prevalence is highest among those 40-59 years of age (Table 13).
|All ages 20 and older||34.9%||33.5%||36.1%|
|60 years and older||35.4%||32.0%||38.1%|
Source: NHANES 2011-2012 54
|TOTAL US POPULATION|
Source: Fryar et al. 20141
Source: Ogden CL et al. 20142
Among all US children aged 2-19 years, the overall prevalence of overweight is 31.8% and obesity 16.9% (Table 14). Cunningham et al. have shown that young overweight children are more likely to have obesity later in life: their prospective study of 7,738 children demonstrated that overweight 5-year-olds were 4 times as likely as normal-weight children to have obesity by age 14.57
2.2 Demographic Differences
There are notable differences in obesity prevalence and risk for comorbidities based on factors that include age, sex, race, ethnicity, and geographic location.58 Differences in obesity prevalence among major ethnic/racial groups in the US are summarized below (Table 16).
|Non-Hispanic white||Non-Hispanic black||Asian||Hispanic|
According to a recent meta-synthesis, obesity disproportionally affects Spanish-speaking women of Central American, South American and Caribbean descent living in the United States.59 In addition, a recent study of patients treated for overweight or obesity in US federally supported health centers reported that overweight patients or patients with obesity were over 2.5 times more likely to be told they had a weight problem if they were Hispanic or Latino.60
Obesity prevalence has also tripled among Asian/Pacific Islander (API) populations over the last two decades, from 3.7% in 1992 to 13.3% in 2010 for all API subgroups (Table 17). Though the overall prevalence remains lower in API populations than non-Hispanic whites, the estimated annual rate of increase in prevalence is higher for APIs: 6.2% versus 4.0% for non-Hispanic whites.61
|Race/ethnicity||Prevalence, 1992-1995||Prevalence, 2006-2011|
Source: Singh and Lin, 201361
ND = no data available.
The risk for overweight and obesity appears to augment among immigrants, with increasing duration of residence in the United States (Table 18).62 In 2003–2008, obesity prevalence ranged from 2.3% for recent Chinese immigrants to 31%–39% for Native Americans, US-born blacks, Mexicans, and Puerto Ricans, and long-term Mexican and Puerto Rican immigrants, as summarized in Table 19. Obesity prevalence for US-born adults increased from 13.9% to 28.7%, whereas prevalence for immigrants increased from 9.5% to 20.7%. The prevalence of obesity among Native American/Alaska Native people was very high, at 39.2%, in 2003-2008.
|Duration of residence in US (years)||Prevalence, 1992-1995||Prevalence, 2003-2008|
Source: Singh GK et al. 201162
|US immigrants by racial group||Prevalence, 2003–2008|
|US immigrants by country of origin|
|Other Asian and Pacific Islanders||4.0%|
|Central, South American, other Hispanics||14.6%|
Source: Singh GK et al. 201162
Among children in the United States, like the adult population, prevalence of obesity is highest among Hispanic and non-Hispanic black populations (Table 20).
|Non-Hispanic white||Non-Hispanic black||Asian||Hispanic|
Source: Ogden CL et al. 20142
These results are corroborated by an observational study conducted by Kaiser Permanente Northern California (KPNC) on obesity prevalence among KPNC members 2–5, 6–11, and 12–19 years of age (Table 21). Prevalence of obesity (BMI ≥ 95th percentile) at 2003–2005 and 2009–2010 was highest among Hispanics/Latinos across all age groups and lowest among Asians at both time points.63
|Kaiser Permanente Northern California members||2003-2005
|02–05||85,804 (33.8%)||137,479 (32.2%)|
|06–11||82,464 (32.5%)||140,815 (33.0%)|
|12–19||85,739 (33.7%)||148,383 (34.8%)|
|Male||128,598 (50.6%)||218,249 (51.1%)|
|Female||125,404 (49.4%)||208,423 (48.9%)|
|Asian||34,413 (13.6%)||63,947 (15.0%)|
|Black||23,179 (9.1%)||34,175 (8.0%)|
|Hispanic/Latino||25,959 (10.2%)||55,977 (13.1%)|
|White||98,449 (38.8%)||153,714 (36.3%)|
|Other||21,660 (8.5%)||40,918 (9.6%)|
|Unknown||50,342 (19.8%)||76,941 (18.0%)|
Source: Gee et al. 201363
Recent analysis of data from the Pediatric Nutrition Surveillance System (2008-2011) by the CDC shows some promise among young children in the US: based on measured weight and height data for nearly 12 million US children of preschool age, there were statistically significant downward trends in obesity in 18 states, and no significant increase in 21 states.64
The latest data (2011-2013) from the CDC’s Behavioral Risk Factor Surveillance Survey (BRFSS) indicate that self-reported obesity rates continue to rise across the United States.65 In total, 18 US states have obesity prevalence rates of 30% or higher (Table 22). Even in states with the lowest prevalence rates, more than one-fifth of their respective populations have obesity.
|States with highest prevalence of obesity||States with lowest prevalence of obesity|
|State||Prevalence, 2011-2013||State||Prevalence, 2011-2013|
Source: Behavioral Risk Factor Surveillance Survey, 2011-201365
As the BRFSS data is self-reported, the actual state-level prevalence of obesity is likely underestimated, because people tend to overestimate their height and underestimate their weight.
The combined negative effects of increasing obesity are projected to reduce mean life expectancy at age 40 (for both men and women) by 0.28 years by 2020, 0.55 years by 2030, and 0.78 years by 2040.66
Among the high-income countries, the US has one of the highest prevalence rates of obesity and one of the lowest life expectancies.67 According to a study that projected the fraction of deaths attributable to obesity, obesity reduced US life expectancy at age 50 years in 2006 by 1.54 years for women and by 1.85 years for men.67 The differences between the population attributable fraction of deaths from obesity in the US was typically greatest at ages 50 to 59 years for both men and women, reflecting the large proportion of US residents with obesity in this age group. For women, the greatest effects were found between 60 and 69 years of age, whereas for men, the impact of obesity was highest at ages 50 to 59 years. At age 50 years, obesity has reduced life expectancy from between 0.88 and 1.54 years for women, and 0.62 to 1.85 years for men.66 Patterns of socioeconomic disparity have been found to relate to 11 health indicators, including life expectancy at age 25 and obesity: across all racial groups, it has been argued that the health problems that accompany obesity are exacerbated by low income and educational level.68
According to a study based on the 1997-2000 National Health Interview Survey of non-smoking US women, women with obesity who have breast cancer stand to lose 1 to 12 years of life, depending on their age, race, and obesity status. The relative risk for death in this population increases with the degree of obesity. Among women with obesity who have breast cancer, those under age 50 across all racial groups were predicted to lose the most life years; racial groups other than whites and blacks lost the most life years (11.9 years), followed by whites (9.8 years) and blacks (9.2 years).69 However, this conclusion may need to be re-evaluated. A recent study of physical activity levels by race, age, and obesity indicates that fewer African-American patients met American Cancer Society guidelines. The authors suggest that disparities in survival among breast cancer patients with obesity correlates with average physical activity levels.70
In 2008, a systematic review of literature from 1966 through 2007 showed a small but significant increase (risk ratio, 1.12) in postmenopausal breast cancer in women with obesity.71 It is hypothesized that in these women, the increase in white adipose tissue allows for increased production of estrogen as compared with women of normal weight. Conversely, a 2012 analysis of the Study of Tamoxifen and Raloxifene (STAR) trial and the Breast Cancer Prevention Trial (BCPT) showed only a modest, statistically non-significant increase in risk for postmenopausal breast cancer correlated with BMI. The authors of that analysis point out that there are other factors besides BMI that might explain the discrepancies, including detection bias. Addressing this conundrum, a recent study applied systems analysis to the variables that possibly affect the prevalence of breast cancer—age, race/ethnicity, age at menarche, age at first birth, age at menopause, obesity, alcohol consumption, income, tobacco use, use of hormone therapy (HT), and BRCA1/2 genotype. The authors applied their analysis to women in the state of California; a 50% decrease in excess BMI would reduce the incidence of invasive breast cancer by 384 cases per 100,000 women over 55 years of age. A 100% decrease in excess BMI would produce a reduction of 375 cases per 100,000.72
According to a 2013 study73, in the year 2000, obesity was associated with nearly 112,000 excess deaths relative to normal weight. In a meta-analysis of white women throughout the world, including the US, grade 1 obesity (BMI 30 to <35) was associated with ~30,000 excess deaths and grades 2 to 3 (BMI ≥35) with more than 82,000 deaths.73 Compared with normal-weight adults, adults with obesity had at least a 20% significantly higher rate of dying of all-cause or cardiovascular disease (CVD). These rates advanced death by 3.7 years (grades 2 and 3) for all-cause mortality and between 1.6 (grade 1) and 5.0 years (grade 3) for CVD-specific mortality. The burden of obesity was greatest among adults aged 45 to 64 years for all-cause and CVD-specific mortality and among women for all-cause mortality.
Using waist circumference as a metric in a pooled study of 650,386 white adults aged 20 to 83 years, a strong positive linear association of waist circumference (WC) with all-cause mortality was observed for men (hazard ratio 1.52 for WC ≥110 vs <90 cm) and women (hazard ratio 1.80 for WC ≥95 vs <70 cm).74 A meta-analysis using more recent data from adequately adjusted studies found that obesity was associated with significantly higher all-cause mortality, with a summary hazard ratio of 1.21 for all grades of obesity combined, 0.97 for grade 1, and 1.34 for grades 2 and 3. Relative to the normal weight category, the hazard ratio for obesity estimated from pooled studies was 1.20 for men and 1.28 for women.75
Overall influence on life expectancy: Obesity as comorbidity
Studies that look at the relationship between increased mortality risks for persons with specific illnesses provide further evidence that obesity is a disease. In a population-based case-control study of men who underwent radical prostatectomy, men with obesity overall experienced greater than 50% increase in prostate cancer mortality, with the strongest effect for men having the most aggressive forms of cancer (Gleason score 8 and higher, adjusted odds ratio 2.37).76
Similarly, a large study that pooled five-year follow-up data for African Americans who died from pancreatic cancer, relative to a BMI 18.5–24.9, those with BMI of 30.0 to 34.9 had an HR of 1.25, and those with BMI ≥35.0 had an HR of 1.31.77 For women who underwent surgery for advanced epithelial ovarian cancer, the obese group (BMI ≥40.0) had a higher adjusted odds ratio for severe complications and a 90-day mortality rate of 15.7%, higher than both underweight and normal to patients with grade 2 obesity.78 Finally, a study that pooled information in 20 prospective studies of adults with obesity, grade 3 obesity was associated with substantially elevated HRs of death and major reductions in life expectancy compared with normal weight: BMI of 40–44.9, 45–49.9, 50–54.9, and 55–59.9 kg/m2 was associated with an estimated 6.5, 8.9, 9.8, and 13.7 years of life lost, respectively.79
During the period 1991–1996, the outpatient use of anti-obesity drugs, mostly phentermine or fenfluramine, in the United States peaked at 8,529 anti-obesity drug prescriptions filled per 100,000 US population. Starting in 1997, prescription rates decreased dramatically when fenfluramine and dexfenfluramine were voluntarily withdrawn from the market due to their association with valvular heart disorders. Whereas the use of phentermine started to increase in 2004 after an earlier decline, this drug has remained the leading prescription weight-loss drug throughout the study period. In 2011, 2,554 anti-obesity drug prescriptions were filled per 100,000 US population, of which 86.6% were for phentermine.80 Table 23 summarizes the distribution of all patients using anti-obesity medication between 2008-2011. Notably, these data are prior to the most recent FDA approvals.
|BMI range||≤ 24.9||25–26.9||27–29.9||≥ 30|
Source: Hampp C et al. 2013 80
Orlistat, a pancreatic lipase inhibitor, was approved in 1999 by the FDA. Until 2012, orlistat was the only anti-obesity drug approved by the FDA for long-term use.22 A number of new pharmacotherapies for obesity management have since come to market, including lorcaserin and phentermine/topiramate in 2012, and most recently naltrexone/bupropion in 2014 and liraglutide in 2015, as treatment options for chronic weight management supplemental to diet and exercise.81 Preliminary studies suggest that naltrexone and buproprion affect two separate areas of the brain that are in involved in food intake. 82 Liraglutide, a GLP-1 inhibitor, at 3 milligrams per day was recently approved by the US FDA and has been approved for anti-obesity use in the EU.83 In a clinical trial [ClinicalTrials.gov ID:NCT01272219], as reported at the 96th annual meeting, of the Endocrine Society, liraglutide induced greater mean weight loss (8.0%) than placebo (2.6%) after 56 weeks; the adverse events were mild and transient. It reduced blood pressure and improved glycemic control.84,85 In existing studies, phentermine/topiramate had a superior weight loss profile to lorcaserin, but the incidence of adverse effects was lower with lorcaserin. Both drugs were well-tolerated, and adverse events were modest in intensity, dose dependent, mild, resolved quickly,86 and tended to decrease with the duration of treatment.87
As shown in Table 24, the rate of bariatric surgery per 100,000 adults increased more than 4-fold between 1998 and 2002; the population-based rate continued to increase to 63.9 in 2004 but plateaued at 54.2 procedures in 2008.
|Gastric bypass (Roux-en-Y)||78%||92%||72%||69%|
|Laparoscopic gastric band||n/a||n/a||24%||29%|
|Overall annual rate/100,000 adultsa||6.3||32.7||36.9||54.2|
|Median age, years||39||42||44||45|
|Chronic liver disease, %||11%||9%||7%||10%|
|Sleep apnea, %||19%||26%||13%||14%|
|In-hospital mortality, %||0.80%||0.50%||0.12%||0.10%|
|Median length of stay, days||4||3||2||2|
Source: Nguyen NT et al. 2013 88
Over 10 years, the number of adolescent inpatient bariatric procedures increased from 328 in 2000 to 1009 in 2009. Adolescent bariatric surgery trends mirror those observed in the adult population, with a plateau in volume during the mid-2000s and a shift toward less invasive procedures.88 One such innovation, sleeve gastrectomy, has been shown effective in producing weight loss.
In 117 patients with a starting mean BMI of 46.6 ± 6.0 kg/m2, laparoscopic gastric band significantly lowered the BMI to 30.3 ± 5.9 kg/m2 and 30.6 ± 5.6 kg/m2 at 12 and 24 months respectively, and resolved obesity-related diseases; at two years, the remission-rate for type 2 diabetes mellitus was 80.7%, hypertension 63.9%.However, there were some complications, including an increase of GERD, from 12.8% prior to the operation to 27.4% at 2 years post-operative.89
One of the first studies to provide a comprehensive comparison of diets randomly assigned 811 overweight adults to diets with four different percentages of fat, protein, and carbohydrates. All participants were offered group and individual instructional sessions for 2 years. Among the 80% of participants who completed the trial, the average weight loss was 4 kg and 14% to 15% of the participants had a reduction of at least 10% of their initial body weight. Satiety, hunger, satisfaction with the diet, and attendance at group sessions were similar for all diets; attendance was strongly associated with weight loss (0.2 kg per session attended). The diets improved lipid-related risk factors and fasting insulin levels. The end result was that clinically meaningful weight loss resulted from reduced-calorie diets, no matter which macronutrient was emphasized.90,91
A recent meta-analysis reviewed sources that make claims for superiority of one diet over others for inducing weight loss (Table 25). Among 59 eligible articles reporting 48 unique randomized trials (including 7,286 individuals) as compared with no diet, the largest weight loss was associated with low-carbohydrate diets and low-fat diets and there was no difference between the effectiveness of these diet categories.
|Diet Type||Weight loss at 6 months||Weight loss at 12 months|
|Low-carbohydrate||8.73 kg||7.25 kg|
|Low-fat||7.99 kg||7.27 kg|
|Moderate macronutrients||6.78 kg||5.70 kg|
|Lifestyle, Exercise, Attitudes, Relationships, and Nutrition (LEARN)||6.07 kg||5.16 kg|
Source: Johnston et al. 201492
In the analysis adjusted for diet class, all treatments were superior to no diet at 6-month follow-up. Significant weight loss was observed with any low-carbohydrate or low-fat diet. Behavioral support and exercise as an add-on to diet appeared to modestly enhance the weight loss effects at the 6-month follow-up, though this association was nonsignificant for behavioural support at 12 months. Overall, the authors concluded that although weight loss differences between individual named diets were small, all treatments were superior to no diet. This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.92
The aforementioned studies also suggest that dietary advice needs to be backed up by ongoing support, and that differences in various dietary approaches might be successful for different persons. Facing that challenge, representatives from the American College of Cardiology, American Heart Association, and The Obesity Society published an extensive evaluation of the components of weight-loss management (hereinafter “the ACC/AHA/TOS guidelines”). The conclusion of the AHA/ACC/TOS guidelines was that caloric restriction is the key mechanism driving weight loss, and in agreement with the results of the two studies mentioned above, acknowledgement of minimal distinction between diets based on different proportions of macronutrients. The panel recommended future research to further examine application of dietary guidelines to specific patient populations according to demographic influences, degree of obesity, diet as a preventive strategy, and baseline co-morbid conditions.47 On the basis of the panel’s meta-analyses, the following table illustrates interventions deemed effective according to studies where strength of evidence was rated as high.
Lesser improvements were found in health profiles where the strength of evidence was moderate. In those overweight and adults with obesity and T2D managed only with a comprehensive lifestyle treatment, there was some weight gain over 4 years. This weight gain resulted in an increase in HbA1c below pre-intervention, but at clinically meaningful levels. In observational cohort studies, showing low strength of evidence, there was a 25% decrease in mortality rate among overweight and adults with obesity and T2D who intentionally lost 9–13 kg compared with weight-stable controls.47
A systematic review of randomized clinical trials showed that exercise alone as a means of weight loss only produced small mean weight loss compared to no treatment. However, when combined with diet, increasing exercise intensity not only increased the weight loss but also resulted in significant positive changes in other metabolic outcome measures: reduced diastolic blood pressure, triglycerides, and fasting glucose.93 Furthermore, the response to exercise, like other weight loss interventions, is highly variable with some individuals losing significant amounts of weight while whereas others do not.
A recent review based on NHANES data in US adults has shown that average caloric intake did not change significantly over the period 1988 to 2010; instead, the main determinant for increasing obesity was a decline in physical activity level.94 The proportion of adults who reported no leisure-time physical activity increased over the period from 19.1% to 51.7% in women, and from 11.4% to 43.5% in men.
Successful pharmacotherapy as an adjunct to diet and exercise provides an additional tool for those persons who are not able to lose weight, or for those in whom obesity has reached a critical stage.46 Drugs to treat obesity can be divided into three groups: those that reduce food intake; those that alter metabolism; and those that increase thermogenesis.97 There is general consensus that weight loss of 5% or more, achieved through intensive lifestyle intervention, is clinically meaningful: it reduces cardiovascular risk factors, prevents or delays development of T2DM, and ameliorates other health consequences of obesity. Based on available evidence to date, the US Preventive Services Task Force (USPSTF) recommends that patients with a BMI of 30 kg/m2 or higher be offered or referred to intensive behavioral interventions.98
Five drugs are currently approved by the US Food and Drug Administration for long-term management of obesity. Outcomes associated with each pharmacotherapy are highlighted below and discussed in greater detail by Apovian et al. 46:
Orlistat, approved in 1999 as a prescription drug and for over-the-counter sale in 2007, partially blocks absorption of fats. In trials, the mean body weight loss was 3% greater than placebo, and patients experienced less weight gain after 2 years.22 The weight loss in a 3 year study was 11% at 1 year compared to 7% for the placebo and after 3 years, the loss was 6.5% in patients as compared with 4.1% for the placebo.86 Side effects can include an increased number of bowel movements and potential changes in the bowel function and microbiota.22
Lorcaserin, a serotonin, dopamine and norepinephrine reuptake inhibitor, was approved by the FDA in 2012. The mean body weight loss for lorcaserin was 5.8 kg vs 2.2 kg for placebo. Side effects include a possible concern for cancer risk.22
Naltrexone/buproprion, approved in 2014, is intended for patients with a BMI of 30 kg/m2 or above, or 27 kg/m2 or greater in the presence of at least one weight-related comorbidity such as hypertension, type 2 diabetes, dyslipidemia.82
Phentermine, an appetite suppressant, was approved for short-term use in 1959; weight loss for patients using this drug was 3.6 kg greater than those treated with a placebo. However, phentermine is approved only for short-term use86, and discontinuation of this drug involves withdrawal symptoms.22 Phentermine/topiramate, a combination of phentermine with topiramate, involves a synergistic action. It was approved in 2012. Using a dosage of 7.5 mg phentermine with 46 mg topiramate produced a reduction in weight of 9.3% versus the placebo at -2.2%. For the combination 15 mg phentermine and 92 mg topiramate, the reduction was as high as 10.75%.22 The most commonly observed side effects in clinical trials were those of the constituent drugs: phentermine causes insomnia and dry mouth early in treatment, but these resolved. Topiramate, a carbonic anhydrase inhibitor, is associated with altered taste for carbonated beverages and tingling in fingers, toes, and perioral areas, and may lead to mild metabolic acidosis.86
Liraglutide, FDA approved in December 2014, is a GLP-receptor agonist. In a European study, the weight loss, depending on a dosage ranging from 1.2 to 3.0 mg, was 4.8 to 7.2kg, versus the placebo at 2.8 kg and 4.1 kg in the orlistat-treated comparator group. Liraglutide remains the only anti-obesity medication approved by the European Medicines Agency.86
A review of nearly 30 long-term studies comparing bariatric procedures showed that gastric bypass surgery had better outcomes than gastric banding for long-term weight loss, controlling T2DM and high blood pressure, and lowering cholesterol levels.99
The authors of the review found that those undergoing gastric bypass operations lost more weight—an average of 66% of their excess weight (which translates to about a 30% loss of body weight)—compared with a 45% average excess weight loss for those undergoing gastric banding procedures (about 22% loss of body weight). In a study of 208 patients with clinically severe obesity (BMI ≤50 kg/m2) who underwent sleeve gastrectomy as a sole procedure at a bariatric referral center, a mean excess weight loss of 71.1% (about 35% weight loss) was documented in 90 (89.4%) of 106 patients, available for follow-up after 3 years. The excess weight loss slowly declined to 57.6% (about 28% weight loss) in 21 (77.7%) of 27 patients at 5 years of follow-up. No deaths were recorded. Early morbidity (≤30 d) was 9.6%, chiefly owing to staple line closure leaks, and late morbidity was 4.8%. The excess weight loss slowly declined to 57.6% in 21 (77.7%) of 27 patients after 5 years of follow-up. No major metabolic deficiencies were apparent. Statistically significant improvements in pre-existing hypertension, diabetes mellitus, and dyslipidemia were achieved. GERD symptoms developed in 9.8% of patients within the first postoperative year but lessened over time to 7.4% at the 5-year mark.100