Overeating doesn’t cause obesity. Obesity causes overeating.”
–Dr. Lee Kaplan, Harvard University

Obesity is a disease.

Image created by OpenAI’s ChatGPT with DALL-E.

We see it everywhere, the very real and ongoing obesity pandemic. This pernicious disease now affects nearly half of the adults in this country, including those on both sides of the hospital bed rails, bringing with it over 200 associated complications and morbidities.

Obesity first became common in America during the last decades of the 20th century; since then its prevalence has only accelerated. Our youth have not been spared, with one in six children and one in four adolescents currently affected.

Despite what we see, many fail to recognize obesity as a true disease with complicated origins. The misguided and reductive idea that behaviors such as eating too much and moving too little are the predominant factors in risk and causation of obesity perpetuates the belief that those suffering with this devastating disease have an underlying character flaw such as gluttony, laziness, or lack of willpower. This in turn propagates societal and medical bias, leading to patient shaming and delayed obesity interventions.

While there’s no standard definition of obesity, it can be aptly described as a chronic, progressive, relapsing, multifactorial, neurobehavioral, inflammatory disease with excessive and dysfunctional body fat mass. Obesity and overweight (‘pre-obesity’) should be considered together as a treatable disease state of disordered fat mass (adiposity).

What causes obesity?

To answer this question, it’s important to properly view fat mass as a complex, metabolic, immune, and endocrine organ that, along with input from the brain, plays a critical role in the body’s energy regulation and survival. Appetite—which drives energy consumption (calories), energy storage (in fat cells, “adipocytes”), and energy metabolism—is regulated by the brain. Appetite is further influenced by satiety and hunger hormones released from the gut, fat, and pancreas, as well as by the brain’s hedonic food reward system (the latter affecting behaviors such as binge eating or carbohydrate addictions). Disruptions in the above processes can lead to overeating and increased fat mass. Most approved anti-obesity medications target appetite regulation.

Why are some of us more affected by obesity and overweight (“pre-obesity”) than others? Genes represent the greatest risk of obesity, but DNA is not destiny. Genetic susceptibility is greatly influenced by an obesogenic environment and other risk factors:

  • Disordered sleep
  • Eating calorie-dense, overly processed foods
  • Lower socioeconomic status
  • Intrauterine trauma
  • Chronic stress
  • Obesogenic drug use (some beta blockers, selective serotonin reuptake inhibitors (SSRIs),  neuropsychiatric drugs, steroids, antihistamines, and others)
  • An evening chronotype (being a “night person”)
  • Endocrine-disrupting chemicals [EDCs])

Having a high polygenetic obesity risk while living in an obesogenic environment can cause epigenetic changes resulting in impaired energy regulation and dysfunctional fat mass. 

The bottom line: having a propensity to develop obesity or pre-obesity is not your fault any more than overdosing on Twinkies causes type 2 diabetes. It’s time to banish the weight bias.

How does obesity affect health?

It didn’t take the COVID-19 pandemic to magnify the significant impact of obesity and overweight on health and disease; the number of hospitalized overweight patients has long been increasing. However, the reported link between increased adiposity and worse COVID outcomes greatly changed the public’s perception. Why, it was asked, are those who are obese or overweight more likely to die from their illness?

The answer: it’s all about fat mass. Obesity occurs when the body accumulates excessive amounts of fat within the subcutaneous space. When the capacity for subcutaneous fat is overwhelmed, hypertrophied and highly inflammatory fat is deposited within ectopic locations, such as the viscera, thorax and muscle. The body may even perversely defend this increased fat mass by increasing hunger, blocking satiety, and reducing resting energy expenditure!

Greatly enlarged fat mass can lead to very high mechanical forces (which can contribute to osteoarthritis, GERD, and other conditions). In addition, the presence of inflammatory, ectopic fat (“sick fat”) results in insulin resistance and multiple metabolic impairments that are associated with numerous complications, including cancer, type 2 diabetes, fatty liver, sleep apnea, cardiometabolic and kidney disease, depression, and early mortality. Being slightly overweight or lean but with central adiposity also conveys high metabolic risk (with fatty liver).

Therefore, the primary focus of obesity management should be on improving metabolic health and quality of life, not simply reducing “numbers on the scale” or fitting into skinny jeans.

Taking obesity seriously, minus the bias.

Recognizing obesity and pre-obesity as a serious disease that must be treated early and aggressively (but without bias) is a good first step. Effective treatment incorporates personalized lifestyle interventions, along with available effective anti-obesity medications like GLP-1 agonists—liraglutide (Saxenda), semaglutide (Wegovy), and tirzepatide (Zepbound) are approved for weight loss, though some other GLP-1 drugs may be prescribed off-label—and surgical options.

(More information about helping patients manage obesity and pre-obesity can be found on the websites of the Obesity Society and the American Association of Clinical Endocrinologists.)

By Christine Kessler, MN, ACCNS, ANP-BC, BC-ADM, FAANP, is the founder and clinical consultant for Metabolic Medicine Associates. As an advanced practice nurse, Christine worked in critical care for 20 years, then as an ANP in general endocrinology for 23 years.