Obesity is Not a Disease of Sloth and Gluttony*
The most recent data from the CDC indicates that approximately 35% of American adults have obesity (1). In order to reduce prevalence of this disease (yes, disease), a popular notion is that people with obesity just need to “eat less and move more.” Indeed, many public health programs use this concept as their primary approach for combating obesity. While eating less and moving more may help prevent obesity or result in successful, sustained weight loss in individuals who are overweight (but not yet obese), ongoing research indicates that these simple lifestyle changes will do very little in the face of prolonged obesity (2).
If you look at any weight loss study, you will most assuredly find the same results, regardless of study design. The first six months are generally characterized by substantial weight loss, followed by sustained weight regain, resulting in a final weight that is negligibly lower and potentially higher than the starting weight . Only about 20% of people who lose weight maintain that weight loss over the following year (3). This “checkmark effect” or weight loss recidivism that has been reported nearly ubiquitously across diet and exercise-based weight loss trials (4) indicates that lifestyle interventions, as they are currently designed and implemented, are generally not successful modalities for treating obesity.
Based on a rudimentary understanding of metabolism, the calories in/out approach should work for weight loss and weight loss maintenance. So why do so many people regain the weight? Is it an issue of willpower? In short, the answer is no.
The answer lies in the complex network linking the environment, genetic predisposition to obesity, as well as metabolic and physiological changes. A large body of literature indicates that the brain’s reward systems are significantly dysregulated in individuals with obesity (5). In an environment that supports ease of access to highly palatable foods, the pleasurable effects of consuming said foods can override homeostatic control of intake. While some people are able to regulate intake despite the high palatability of these foods, a number of genetic mutations in the brain’s reward systems may result in overeating and obesity in many people. Furthermore, the hypersensitive reward systems that often lead to obesity can become insensitive once a state of obesity is attained. In effect, this leads to overeating to receive the same reward from the same foods. These dysregulated reward systems are coupled with preadipocyte (young fat cell) expansion into mature adipocytes, allowing for increased fat storage. While this isn’t the entire story, this should shed some light on the complex interactions of dysregulated internal systems that foster the metabolic abnormalities that result in obesity. Importantly though, these impairments are typically only demonstrated once obesity has been introduced and sustained (4) and individuals who are overweight (but not obese) will likely not encounter many of these aberrations.
As for weight loss, when caloric restriction is initiated, the body triggers a number of systems to prevent starvation. From an evolutionary perspective, this makes sense as food sources were often unpredictable and the body adapted to conserve energy – the “feast and famine” principle. However, for most of us living in industrialized nations, famine is rare and feast is common, limiting the need for this once very necessary adaptation (however, the body has not evolved to recognize the abundance of calories in our modern food supply). When we try to induce weight loss via caloric restriction, the body will reduce its resting metabolic rate to counter these advances (6). This supports the “set point theory” – the idea that the body will defend its highest-sustained weight. In fact, as weight loss increases, the drive to restore the highest bodyweight only increases (7).
All of these biological adaptations that introduce, sustain, and defend obesity explain why weight loss and its maintenance is so exhaustingly difficult for so many people. In a commentary published in 2015 in Lancet: Diabetes and Endocrinology, Ochner and colleagues suggest that most individuals who have had obesity but lost weight simply have “obesity in remission and are biologically very different from individuals of the same age, sex, and body weight who never had obesity.” Hypothetically, imagine you are comparing two people: they weigh the same, but person A had obesity and has lost weight whereas person B has never lost weight. Person A will have to burn up to 300 more calories (or consume 300 fewer calories) than person B to maintain that weight (2). This underscores the idea that weight regain is not simply an issue of willpower and weakness.
What we need more of are studies evaluating multiple approaches to weight loss (perhaps diet and exercise studies with more innovative approaches to maintain weight loss; surgeries, medications, likely in combination with lifestyle changes). What we need less of is bias from people without obesity, the media, and even healthcare providers. Indeed, “the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely” (2). We also need better obesity prevention approaches because, clearly, it’s biologically more feasible to prevent weight gain than to lose weight and keep it off.
- Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adults obesity in the United States, 2011-2012. JAMA. 2014;311(8):806-814. doi:10.1001/jama.2014.732.
- Ochner CN, Tsai AG, Kushner RF, Wadden TA. Treating obesity seriously: when recommendations for lifestyle change confront biological adaptations. Lancet Diabetes Endocrinol. 2015:
- Wing RR, Phelan S. Long-term weight loss maintenance. Am J Clin Nutr (2005) 82:222S-225S.
- Ochner CN, Barrios DM, Lee CD, Pi-Sunyer FX. Biological mechanisms that promote weight regain following weight loss in obese humans. Physiol Behav. 2013:120:106-13. doi: 10.1016/j.physbeh.2013.07.009.
- Kenny JP. Reward mechanisms in obesity: new insights and future directions. Neuron. 2011:69(4):664-79. doi:10.1016/j.neuron.2011.02.016
- Grattan BJ, Connolly-Schoonen J. Addressing Weight Loss Recidivism: A Clinical Focus on Metabolic Rate and the Psychological Aspects of Obesity. ISNR Obesity. 2012. doi:10.5402/2012/567530
- Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes. 2010:34:S47-55. doi:10.1038/ijo.2010.184
*Originally published in another form on the ASN Blog.
Photo by Skitter Photo on stocksnap.io