Understanding Obesity: Classification, Etiology, and Epidemiology
The word ‘obesity’ is used by providers, patients, media outlets, and advertisers so frequently that we rarely consider what it really means from a clinical perspective. How is it measured? How is it affected by genetics, lifestyle, and environmental factors? In this article on understanding obesity, you’ll learn more about this complex, chronic condition.
Obesity in adults is defined as a body-mass index (BMI) >/=30 kg/m2 whereas overweight is defined as a BMI >/= 25 kg/m2. BMI is often used to classify weight status in epidemiologic (population-based) studies and in clinical practice settings, however, it is a surrogate measure of adiposity (body fat) in that it does not distinguish between tissue type (adipose [fat mass] versus non-adipose [lean mass]). Thus, a well-trained athlete with a BMI of 30 may not have excess body fat. Patterns of fat distribution are also important to consider. Specifically, individual variation in body fat distribution is a major clinical variable explaining the metabolic heterogeneity of obesity and its related cardiovascular risk. Evidence suggests that individuals who are obese (as defined by BMI >/= 30) with excess visceral (abdominal) fat are at greater risk of developing metabolic complications predictive of increased risk for cardiovascular disease (CVD).1 Taken together, evidence points to the need for clinicians to go beyond assessment and monitoring of BMI in patients who present with obesity and also assess distribution of body fat. Measurement and monitoring of waist circumference is recommended, as well as assessment and management of established risk factors for CVD.2
Etiology of Obesity
The emergence and persistence of obesity, a chronic condition, is attributed to many factors. Importantly, obesity is viewed as a complex, multifactorial condition influenced by the interaction of genetic factors and potentially modifiable behaviors and environments. The contribution of genetic factors to obesity, referred to as “heritability,” has received substantial research attention. Family, twin, and adoption studies led to the identification of some causal genes in monogenic forms of obesity; however, the increase in the global prevalence of this chronic condition in the past several decades points to consideration of other etiologies because the human genome is not likely to change in such a short time frame. In addition, and noteworthy, is that genome-wide association studies (GWAS) and other research approaches have identified many loci related to obesity or BMI; however, the identified variants explain only a small proportion of the heritability of this chronic condition.3
The interplay of genetic and potentially modifiable behavioral and environmental factors has been the focus of more recent investigations designed to guide and inform more individualized, personalized obesity prevention and management. Specifically, epigenetics has emerged as one of the promising areas of current and future research focused on both the prevention and management of chronic conditions including obesity. Broadly defined, epigenetics is the study of heritable changes in gene expression that result in phenotype (observable) variations without changes in actual DNA sequence. Factors such as age, diet, and environmental exposures, as well as disease status, can influence epigenetic changes. The emergence of epigenetic profiles that will contribute to the creation of individual microbiomes and susceptibility to the development of obesity (and other conditions) has been observed in fetal age and is influenced by maternal diet during pregnancy. Indeed, several studies have shown that a healthy diet positively influences the individual epigenetic profile. For example, it has been shown that normal-weight and non-diabetic individuals have epigenetic profiles that are different from their obese and diabetic counterparts. Other risk factors associated with obesity including hyperglycemia, inflammation, endocrine disorders, hypoxia, and oxidative stress appear to be involved in epigenetic changes that influence the development of adiposity as well as insulin sensitivity.3
It is well-established that the development of obesity is influenced by an imbalance between energy intake (calories consumed) and energy expenditure. Health behaviors, particularly patterns of dietary intake and physical activity (including sedentary behaviors) are key contributors to energy balance and critically important to assess and monitor in both preventive and therapeutic interventions focused on overweight and obesity. The adoption of heart-healthy patterns of these behaviors, central to maintaining optimal weight status, begins early in childhood. The family and home environment, including family meals and family activities, are key factors in both the adoption and maintenance of healthy patterns of dietary intake and physical activity.
Unfortunately, not all families have access to healthy foods or safe outlets for physical activity. The availability and affordability of healthy foods has received much attention in recent years with clinicians and public health advocates supporting multi-level initiatives designed to decrease food deserts and enhance sources and options for individuals and families, particularly those residing in under-resourced communities. Similarly, advocacy efforts focused on enabling physically active lifestyles for all are in progress. Taken together, the evidence, as well as anecdotal observations, underscore the importance of looking beyond the level of the individual in considering “best practices” for promoting healthy behaviors and preventing overweight and obesity. As health care providers, attention to the social determinants of health must be considered in patient encounters. Indeed, where people are born, live, school, and work, as well as the policies that impact those environments, are important to optimal health across the life course.
Epidemiology of Obesity
The epidemiology of obesity–the determinants and distribution of this chronic condition–is presented below with emphasis on the U.S. population. Of note, however, is that over the last several decades, the prevalence of overweight and obesity in children and adults has increased globally. Recent data from the National Health and Nutrition Examination Surveys (NHANES), summarized by the American Heart Association (AHA),4 indicate that the overall prevalence of obesity and severe obesity in youth 2 to 19 years of age increased from 13.9% to 19.3% and 2.6% to 6.1% between 1999 to 2000 and 2017 to 2018. Over this same time period, the prevalence of obesity and severe obesity increased from 14.0% to 20.5% and from 3.7% to 6.9% for males, and from 13.8% to 18.0% and from 3.6% to 5.2% for females. Among adults, NHANES data indicate from 1999-2000 through 2017-2018 the prevalence of obesity increased from 27.5% to 43.0%, while severe obesity increased from 3.1% to 6.9%. Among females, the prevalence of obesity increased from 33.4% to 41.9% and severe obesity increased from 6.2% to 11.5%. Of note, significant increases in the prevalence of obesity were observed between 1999 to 2000 through 2017 to 2018 in all age-race and ethnicity groups except for Non-Hispanic Black males, in whom the prevalence increased 1999 through 2006.4
The patterns and trends in the prevalence of obesity as well as severe obesity provide substantial cause for concern and do not bode well for cardiovascular health currently and going forward. Importantly, patterns of obesity prevalence include disparities by race/ethnicity. Obesity has increased among adolescents driven primarily by increases in non-Hispanic Black and Mexican American youth. Obesity and severe obesity, as noted above, have increased among adult men and women with no changes observed among non-Hispanic Black men after the 2005-2006 time point; however, a more rapid increase has been observed in Mexican American than in non-Hispanic white men.4 Important to emphasize is that risks of having obesity and associated comorbidities are conditioned by adverse social-environmental circumstances. Indeed, social disadvantage translates to a greater likelihood of living in neighborhoods with fewer options for healthy eating and physical activity. Collectively, the patterns and trends in obesity and severe obesity persuade us to adopt an equity-oriented obesity prevention framework.5 By definition and design, this calls for consideration and action relevant to social determinants of health and social justice.
Clinical Recap: Understanding Obesity
- BMI is just one data point for measuring obesity; distribution of body fat is another key factor. Recommendations include measurement and monitoring of waist circumference and assessment and management of established risk factors for CVD.
- Obesity is a complex, multifactorial condition influenced by the interaction of genetic factors and potentially modifiable behaviors and environments, which requires a multi-faceted management process.
- Social determinants of health—where people are born, live, school, and work—significantly impact obesity healthy impacts and outcomes.
- Rates of obesity continue to rise across the U.S. and the globe, particularly in non-white populations. Addressing obesity requires local, regional, national, and international strategies.
Related Articles on Understanding Obesity
- Talking About Obesity
- Social Determinants of Health and Obesity
- Maternal Obesity and Cardiovascular Health
- Apovian CM, Gokce N. Obesity and cardiovascular disease. Circulation. 2017;125 (9):1178-1182.
- Arnett D, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease. Circulation. 2019;140(110):e596-e646.
- Thaker VV. Genetic and epigenetic causes of obesity. Adolescent Medicine State of Art Review. 2017;28(2):379-405.
- Tsao CW, Aday AW, Almarzooq ZI, et al. Heart disease and stroke statistics. Circulation. Published online ahead of print, January 26, 2022. doi: 10.1161/CIR00000000000001052.
- Kumanyika S. A framework for increasing equity impact in obesity prevention. American Journal of Public Health. 2019;109(10):1350-1357.